One of the most important experiments in evolution is going on right now in a laboratory in Michigan State University. A dozen flasks full of E. coli are sloshing around on a gently rocking table. The bacteria in those flasks has been evolving since 1988–for over 44,000 generations. And because they’ve been so carefully observed all that time, they’ve revealed some important lessons about how evolution works.

The experiment was launched by MSU biologist Richard Lenski. I wrote about Lenski’s work last year in the New York Times, and in more detail my new book Microcosm. Lenski started off with a single microbe. It divided a few times into identical clones, from which Lenski started 12 colonies. He kept each of these 12 lines in its own flask. Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. And on and on and on, for 20 years and running.

Based on what scientists already knew about evolution, Lenski expected that the bacteria would experience natural selection in their new environment. In each generation, some of the microbes would mutate. Most of the mutations would be harmful, killing the bacteria or making them grow more slowly. Others would be beneficial allowing them to breed faster in their new environment. They would gradually dominate the population, only to be replaced when a new mutation arose to produce an even fitter sort of microbe.

Lenski used a simple but elegant method to find out if this would happen. He froze some of the original bacteria in each line, and then froze bacteria every 500 generations. Whenever he was so inclined, he could go back into this fossil record and thaw out some bacteria, bringing them back to life. By putting the newest bacteria in his lines in a flask along with their ancestors, for example, he could compare how well the bacteria had adapted to the environment he had created.

Over the generations, in fits and starts, the bacteria did indeed evolve into faster breeders. The bacteria in the flasks today breed 75% faster on average than their original ancestor. Lenski and his colleagues have pinpointed some of the genes that have evolved along the way; in some cases, for example, the same gene has changed in almost every line, but it has mutated in a different spot in each case. Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose, they’ve gotten worse at feeding on some other kinds of sugars.

Last year Lenski was elected to the National Academy of Sciences. This week he is publishing an inaugural paper in the Proceedings of the National Academy of Sciences with his student Zachary Blount and postdoc Christina Borland. Lenski told me about the discovery behind the paper when I first met him a few years ago. He was clearly excited, but he wasn’t ready to go public. There were still a lot of tests to run to understand exactly what had happened to the bacteria.

Now they’re sure. Out of the blue, their bacteria had abandoned Lenski’s their glucose-only diet and had evolved a new way to eat.

After 33,127 generations Lenski and his students noticed something strange in one of the colonies. The flask started to turn cloudy. This happens sometimes when contaminating bacteria slip into a flask and start feeding on a compound in the broth known as citrate. Citrate is made up of carbon, hydrogen, and oxygen; it’s essentially the same as the citric acid that makes lemons tart. Our own cells produce citrate in the long chain of chemical reactions that lets us draw energy from food. Many species of bacteria can eat citrate, but in an oxygen-rich environment like Lenski’s lab, E. coli can’t. The problem is that the bacteria can’t pull the molecule in through their membranes. In fact, their failure has long been one of the defining hallmarks of E. coli as a species.

If citrate-eating bacteria invade the flasks, however, they can feast on the abundant citrate, and their exploding population turns the flask cloudy. This has only happened rarely in Lenski’s experiment, and when it does, he and his colleagues throw out the flask and start the line again from its most recently frozen ancestors.

But in one remarkable case, however, they discovered that a flask had turned cloudy without any contamination. It was E. coli chowing down on the citrate. The researchers found that when they put the bacteria in pure citrate, the microbes could thrive on it as their sole source of carbon.

In nature, there have been a few reports of E. coli that can feed on citrate. But these oddballs all acquired a ring of DNA called a plasmid from some other species of bacteria. Lenski selected a strain of E. coli for his experiments that doesn’t have any plasmids, there were no other bacteria in the experiment, and the evolved bacteria remain plasmid-free. So the only explanation was that this one line of E. coli had evolved the ability to eat citrate on its own.

Blount took on the job of figuring out what happened. He first tried to figure out when it happened. He went back through the ancestral stocks to see if they included any citrate-eaters. For the first 31,000 generations, he could find none. Then, in generation 31,500, they made up 0.5% of the population. Their population rose to 19% in the next 1000 generations, but then they nearly vanished at generation 33,000. But in the next 120 generations or so, the citrate-eaters went berserk, coming to dominate the population.

This rise and fall and rise suggests that the evolution of citrate-eating was not a one-mutation affair. The first mutation (or mutations) allowed the bacteria to eat citrate, but they were outcompeted by some glucose-eating mutants that still had the upper hand. Only after they mutated further did their citrate-eating become a recipe for success.

The scientists wondered if other lines of E. coli carried some of these invisible populations of weak citrate-eaters. They didn’t. This was quite remarkable. As I said earlier, Lenski’s research has shown that in many ways, evolution is repeatable. The 12 lines tend to evolve in the same direction. (They even tend to get plump, for reasons yet to be understood.) Often these parallel changes are the result of changes to the same genes. And yet when it comes to citrate-eating, evolution seems to have produced a fluke.

To gauge the flukiness of the citrate-eaters, Blount and Lenski replayed evolution. They grew new populations from 12 time points in the 33,000-generations of pre-citrate-eating bacteria. They let the bacteria evolve for thousands of generations, monitoring them for any signs of citrate-eating. They then transferred the bacteria to Petri dishes with nothing but citrate to eat. All told, they tested 40 trillion cells. Here’s a movie of what that looks like…

Out of that staggering hoard of bacteria, only a handful of citrate-eating mutants arose. None of the original ancestors or early predecessors gave rise to citrate-eaters; only later stages in the line could–mostly from 27,000 generations or beyond. Still, even among these later E. coli, the odds of evolving into a citrate-eater was staggeringly low, on the order of one-in-a-trillion.

Now the scientists must determine the precise genetic steps these bacteria took to evolve from glucose-eaters to citrate-eaters. In order to eat a particular molecule, E. coli needs a special channel in its membranes through which to draw it. It’s possible, for example, that a channel dedicated to some other molecule mutated into a form that could also take in citrate. Later mutations could have fine-tuned it so that it could suck in citrate quickly.

If E. coli is defined as a species that can’t eat citrate, does that mean that Lenski’s team has witnessed the origin of a new species? The question is actually murkier than it seems, because the traditional concept of species doesn’t fit bacteria very comfortably. (For the details, check out my new article on Scientific American, “What is a Species?”) In nature, E. coli swaps lots of genes with other species. In just the past 15 years or so, for example, one disease-causing strain of E. coli acquired hundreds of genes not found in closely related E. coli strains. (See my recent article in Slate.) Another hallmark of E. coli is its ability to break down lactose, the sugar in milk. But several strains have lost the ability to break it down. (In fact, these strains were originally given a different name–Shigella–until scientists realized that they were just weird strains of E. coli.)

Nevertheless, Lenski and his colleagues have witnessed a significant change. And their new paper makes clear that just because the odds of such a significant change are incredibly rare doesn’t mean that it can’t happen. Natural selection, in fact, ensures that sometimes it does. And, finally, it demonstrates that after twenty years, Lenski’s invisible dynasty still has some surprises in store.

There are 328 Comments. Add Yours.

Got to love a longitudinal study. This was a very interesting article.

BTW, I’ve got a request out for the Smithsonian Guide to Human Origins in my library queue. Should have it in a day or two. Got to love the inter-library loan system in this state.

Hugo
June 3, 2008

Pure awesome.

NP
June 3, 2008

It’s a fascinating discovery and thank you for providing an excellent summary.

I’m now really looking forward to seeing them isolate the protein(s) involved in this novel trait, and the genetic mechanisms that led to its evolution. It’s great that they’ve been able to document the history of each line, and can just thaw out the ancestral bacteria to do any molecular experiments to answer some of the interesting questions that their discovery raises.

Paul C
June 3, 2008

This is fascinating stuff! I work in a lab undertaking some of the questions that underlie the results obtained. We study the marine bacteria SAR11 and some of the experiments we are in the process of conducting may shed a lot of light on the question of how this one-in-a-trillion chance actually maps out nucleotide by nucleotide. Perhaps natural selection is orders of magnitude more efficient then we ever thought…just think: If this is a one-in-a-trillion chance for one lineage in one lab, and there are an almost unimaginable number of lineages in nature…you do the math. Can’t wait to read the paper…and see the genomes (if it’s in the works).

Ron
June 3, 2008

Link to the paper is broken. (At least for me. PNAS is notorious for having press releases on papers you can’t find for a number of days).

Just finished Microcosm. Excellent book. Off to the book club to see if there’s anything new over there about it.

See, it’s stuff like this that’s totally re-igniting my interest in the sciences. Not that I’d lost interest, really – I just tucked it away as if it was a former life. Not so, anymore. This is, in part, due to intriguing writing like yours and partly because I forgot how much unexpected fun like this work can come from coli.

Re: species… Species distinctions have always seemed a bit fuzzy to me, anyways. When it gets down to precise divisions between species, it sort of feels like a semantic argument with different opinions arising due to what particular aspect of an organism an individual thinks in important.

I wonder if it’s going to come down to whole genome comparisons as the only way to be definitive. But even then…

Mike Haubrich, FCD
June 3, 2008

Clear as mud:

This excites me as much as it does you, and for the same reasons.

One of the things that has struck me in the writings on the species concept is that it is difficult because in defining species we are trying to create a discrete threshhold where none exists in nature. In trying to impose our own limits of imagination on nature, we are never going to be able to come up with “One size fits all” definition. The definition we learned in high school regarding viable, interbreeding offspring only ever applied to sexual reproduction.

Carl – thanks for this post. It has made my day, believe it or not.

Matt
June 3, 2008

Wow, what a fantastic study and lucid summary. Thanks Carl, this is the most excited I’ve been about biology in a while.

A question: how are they sure this citrate eating adaptation was a result of mutations, and not, say, an existing sequence of dna that was just locked in an intron or something, and then eventually shuffled to a coding region of the genome? Could they follow the genetic changes point by point, or are they still trying to figure that out?

Baka
June 3, 2008

Matt,

It sounds to me like that’s precisely what Lenski and his colleagues are planning on doing next. It could be any number of things, or any combination of them, that has resulted in the acquired functionality. It would not surprise me if, in the experiment described where they looked for lines that re-evolved the same citrate-eating functionality, there were different (though perhaps similar) mutations leading to the same result.

I’m sure that what’s going on currently is an analysis of the sequences of the various lines over the generations that saw the rise of this new function to show exactly what happened when. After that’s done, the protein work will need to be done to show how what happened at the sequence level altered the proteins involved.

This is really cool stuff!

RBH
June 3, 2008

In a way some of these results were prefigured in the Avida work (PDF) published by Lenski and colleagues in 2003. For example, there’s this finding:

in some cases, for example, the same gene has changed in almost every line, but it has mutated in a different spot in each case.

In the 2003 work they found that multiple lineages of digital critters evolved to perform the same logic function, but did so by different evolutionary trajectories through gene space.

Then there’s this:

The first mutation (or mutations) allowed the bacteria to eat citrate, but they were outcompeted by some glucose-eating mutants that still had the upper hand. Only after they mutated further did their citrate-eating become a recipe for success.

One sees the same pattern in the evolutionary histories of the Avida runs.

Further, my own analysis of the mutation by mutation trajectory of one of those Avida evolutionary histories shows that a fair number of mutations (25% or more) in the Avida runs are selectively neutral when they first occur, and only generations later are incorporated (after more mutations in other parts of the digital critters’ code) into instruction strings that perform selectively advantageous functions. Teasing out those variables in E. coli is going to be a task!

Matt
June 3, 2008

Thanks, Baka. Very exciting stuff.

Siamang
June 3, 2008

creationist “yeah, but it’s still just a bacteria. Let me know when a bacteria evolves into a dog or a cat.” /creationist

clear as mud
June 3, 2008

@Matt: Hmmm, my memory is E. coli doesn’t really do introns, though I’ve been out of the loop for a few years, so my mind has atrophied.

I’m gonna take a stab at a bad guess. Start with the DNA coding for a component of a nutrient uptake system that coli *does* have.
It could either be:
(1) one that isn’t required under the specific lab conditions, so it’s ok to alter without affecting viability. or
(2) it could be a total gene duplication – which happens plenty enough, if I recall – allowing a copy to be maintained while the other becomes a target for tinkering.

What would be needed is an alteration possibly in the active site which normally binds to a different organic compound.

If there’s enough of a tweak that, suddenly, the active site gains even a bit of new affinity for citrate, then – BINGO – that bug gets the upper hand – it has a new carbon source all to itself.

It can start as just a barely passable uptake system, but it could give the bug’s descendants a toe-hold. From there, if the bug (and the gene) can endure over time, more tweaking would result in further overtaking of the population.

Or not.

I’m waiting to see the paper

Ron
June 3, 2008

Haven’t seen the paper, but I’m willing to speculate a little….

I think we can rule out horizontal gene transfer, as these were supposedly “pure” E. coli lines. My semi-naive speculation is that it is a known transport system that mutated such that it can now move citrate across the membrane effectively plus some additional mutations (in other genes) to effectively metabolize citrate (my metabolic biochemistry is extremely rusty). So I’d agree with clear as mud to some extent. As to the exact nature of the events (mutation vs duplication and mutation), we’ll have to wait for a comment from someone who knows or the paper. I think it is pretty clear that it is multiple events, though.

phisrow
June 3, 2008

This is a really cool result(and a useful reminder that one-in-a-billion is only a synonym for “not happening” on a human scale). I’ll be interested to see what they end up learning about the nature of the change that gave these guys citrate metabolism.

More broadly, how common are experiments of this scale and duration? You hear about 20 odd year studies on human populations from time to time; but how many situations like this one do we have bubbling away?

ramiro quai
June 3, 2008

I am not sure this is the place to post this, but carlzimmer.com is blocked by Firefox 3 as a reported attack site.

Thank you, thank you, thank you. This has made my evening, and reinvigorated my love for and interest in biology.

Brian

Josh
June 3, 2008

horde not hoard

Ian
June 4, 2008

Carl – Are you aware of any long-running experiments like this where the initial bacterium has accumulated sufficient mutations that in the end it would be classified as a different type (genus or something higher) of bacterium from what it started out? The “Shigella” comment in the article above comes close.

I’m tired of the creationists claiming this never happens. It would be nice if there were one of these marathon bacterial studies which had something like this as a result, whether intended or not.

Heather
June 4, 2008

I’m not knowledgeable about bacteriology, nor am I opposed to evolution, but 2 facts in the article stand out: (1) contamination from foreign bacteria, including citrate-eaters, occurred often enough that the researchers had a procedure for it (toss the flask and start from the most recent frozen sample of the same line), and (2) the E Coli. can develop the ability to eat citrate by acquiring the plasmid DNA ring from a citrate-eater.

These facts cause several questions to arise that must be answered before we can start claiming to have “proven” evoloution:
*If contamination occurred from citrate-eaters was identified by the flasks becoming cloudy, how did the researchers ensure that there wasn’t also contamination by other bacteria that don’t conveniently provide visual presence?
*Could it be that there were citrate-eaters present, in a population too small for detection, in the flask, at the time it was frozen? In other words, is it possible that the last frozen sample was in some cases already itself contaminated?
*If the E coli can develop the ability to eat citrate by acquiring plasmids from citrate-eaters, is there perhaps another mechanism by which they could have acquired this ability? Since we know that contamination by foreign bacteria DID occur, I don’t see how this can be ruled out.

I would greatly love to see this experiment repeated in such a way as to rule out contamination by other bacteria.

Ken Finley
June 4, 2008

This is total horse crap. There’s nothing in the Bible to suggest that evolution exists. You’re just arbitrarily making up excuses.

If the bacteria changed, it was clearly because God willed it. He does that sometimes, you know.

Just because God helped the bacteria survived, you can’t just simply say it’s because we come from monkeys. That’s stupid and arrogant.

You’ll go to hell for your blasphemy.

Nate
June 4, 2008

This is a very interesting study, but I would like to point out to some people that seem to have misunderstood what happened. The bacteria did not develop a way to eat citrate, they mutated to a point where they were able to get it across their membranes. They already had the capability to digest it. Most likely a few bacteria had a few mutations which damaged their membranes and allowed citrate to get through. I would like to know what all the tradeoffs were in these bacteria as well. Losing several capabilities while gaining one doesn’t seem like a step forward to me, but in this situation it was advantageous to these bacteria because of the abundance of citrate.

Enlightenment
June 4, 2008

Excellent proof of evolution…but all the bible bangers can’t handle the truth…so they won’t believe in scientific proof…but will instead believe in some imaginary god which is no different than childrens imaginary friends.

Lachlan
June 4, 2008

Even though my education on biology pretty much stopped when I graduated from high school all those years back, I can still identify that this is a fantastically astounding result. A very good read.

@Nate
In terms of fitness in their environment it is of course a step forward.

Nate
June 4, 2008

Enlightenment,
This is a very novel and significant finding. However, it is not a proof for anything, especially that God doesn’t exist. If it is proof for anything is seems fairly obvious that it’s proof that an organism cannot gain a capability through mutations without losing several others. If, hypothetically, the same bacteria gained a dozen more capabilities, this research would tend to show that the bacteria would end up losing 3-4 times that many capabilities. If a bateria did lose that many, it would most likely no longer be viable. It does prove microevolution occurs, which we already knew, but cannot be made to prove anything past that. That type or extrapolation is foolish and ignorant.

clear as mud
June 4, 2008

My goodness, who knew E. coli could bring out the anti-science brigades.

“If it is proof for anything is seems fairly obvious that it’s proof that an organism cannot gain a capability through mutations without losing several others.”

Where on Earth did you get that from? Which abilities did they lose… or gain for that matter? Have you read the paper? I don’t think most anyone else has since it hasn’t been released yet.

Yes, making leaps in logic is a problem all people must combat. This result (whatever the specifics) is not a “disproof of God”. Nor is it proof of what you suggested. “Disproves God!” and “Microevolution!” are keywords of people on different sides using their pre-conceived ideas to jump over the logic presented by the facts before them.

Joshua Zelinsky
June 4, 2008

Heather, I’m not a bacteriologist either but I’ll try to answer your questions:

“If contamination occurred from citrate-eaters was identified by the flasks becoming cloudy, how did the researchers ensure that there wasn’t also contamination by other bacteria that don’t conveniently provide visual presence?” They did determine that the resulting E. coli were able to in fact digest citrate. They confirmed that these were E. coli.

“Could it be that there were citrate-eaters present, in a population too small for detection, in the flask, at the time it was frozen? In other words, is it possible that the last frozen sample was in some cases already itself contaminated?” This is unlikely, since they were able to essentially take the frozen flasks and rerun the experiment. They found(as I understand it. The paper still does not seem to be generally accessible) that the when one reran the experiment with the frozen flasks they sometimes evolved citrate digestion and sometimes did not.

“If the E coli can develop the ability to eat citrate by acquiring plasmids from citrate-eaters, is there perhaps another mechanism by which they could have acquired this ability? Since we know that contamination by foreign bacteria DID occur, I don’t see how this can be ruled out.” It is possible but unlikely given the evidence that it appeared to take multiple mutations. Hopefully followup work will find the specific genes responsible for this in which case we will be able to tell pretty clearly if these are pre-existing E. coli genes or not.

Cale
June 4, 2008

Amazing article reminds me of how fascinated I am with science and biology.

Nate
June 4, 2008

Clear as Mud,
I am completely pro-science. That’s why I said what I did. I work in a lab doing research. What do you do? Did you read the article?
“Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose, they’ve gotten worse at feeding on some other kinds of sugars.”
So, I was simply pointing this out that while the bacteria were now able to uptake citrate they were losing other capabilities. I was also simply trying to limit the wrong extrapolations on both sides. Science by definition cannot prove the existance or non-existance of God, whether that God is Jehovah, Ala, or Vishnu. Also, data can only support or reject hypothesis, it cannot prove anything. So, I should have said this data supports the idea of evolution through mutation on a micro scale. Is that a correct statement or not? This is a fascinating discovery and I look forward to reading the paper.

James E. Tribble
June 4, 2008

Sterling report. Thanks, James

Ray
June 4, 2008

Ah yes. Small steps over 20 years are feasible, but small steps adding into significant changes over millions of years are completely unreasonable.

George Watson
June 4, 2008

wow the immediate thing that strikes me is that the cultures differ in exposure to light based on their placement in the stack.
the energy of light especially certain type of fluorescent bulbs can strike gene molecules and cause mutation.

the mutation rates should be plotted based on exposure to the outside (more lite part ) of the stacks

Mel
June 4, 2008

George,

I think the movie is of what was done with the plates after they were used in the experiment, and not of an experiment itself. The experiments were probably done in a light-free incubator, anyway.

Mel

Interrobang
June 4, 2008

a useful reminder that one-in-a-billion is only a synonym for “not happening” on a human scale

Statistically speaking, a “one in a billion” chance of something on a human scale gives you six to seven people with that something in the world. So anybody who’s using it as a synonym for “not happening” needs to reboot their cliche server.

Bill
June 4, 2008

My first thought after reading about this experiment was, wow think what would happen if this population of bacteria was exposed to a multitude of different environments for a few hundred million years. Imagine what might develop.

Torbj�rn Larsson, OM
June 4, 2008

Statistically speaking, a “one in a billion” chance of something on a human scale gives you six to seven people with that something in the world. So anybody who’s using it as a synonym for “not happening” needs to reboot their cliche server.

Or when the dealer shuffles the cards, the deck will have ~ 1:10^68 chance of that order. [If the shuffle is perfect; there is no such thing of course.] I would say that anybody who’s using it as such a synonym needs to reboot their math server.

ROBERT MUISE (Dramatization): Now, Dr. Minnich, a complaint that’s often brought up – and plaintiffs’ experts have brought it up in this case – is that intelligent design is not testable. It’s not falsifiable. Would you agree with that claim?

SCOTT A. MINNICH (Dramatization): No, I don’t. I have a quote from Mike Behe: “In fact, intelligent design is open to direct experimental rebuttal. To falsify such a claim, a scientist could go into the laboratory, place a bacterial species lacking a flagellum under some selective pressure, for motility, say, grow it for 10,000 generations and see if a flagellum or any equally complex system was produced. If that happened my claims would be neatly disproven.”

ROBERT MUISE (Dramatization): Is that an experiment that you would do?

SCOTT A. MINNICH (Dramatization): You know, I think about it. I’d be intrigued to do it. I wouldn’t expect it to work. But that’s my bias.

Faith
June 4, 2008

Finley, you’d get farther by practicing your religion (and mine) of loving your neighbor as….Never knew anybody to be persuaded by such vitriol as yours. Breathe man, God can handle this His way not yours.

David Harmon
June 4, 2008

Interrobang: Statistically speaking, a “one in a billion” chance of something on a human scale gives you six to seven people with that something in the world.

And similarly, per Paul C, this may well have been a one-in-a-trillion chance, but they had 40 trillion bacteria!

… needs to reboot their cliche server. LOL!

Josh: Actually, it was critical to this experiment, that they were in fact hoarding their horde!

someone
June 5, 2008

Reading this I was taken back to the book ‘Artificial Life’ by Steven Levy where the very same thing was observed through computer generated evolution. A recommended read for those interested.

fazlinnazli
June 5, 2008

Very interesting article. Maybe we need to conserve the population of bacteria same as we conserve the flora and fauna.

Luna_the_cat
June 5, 2008

Matt @ #8 — prokaryotes like E. coli don’t, as a rule, have introns. They have a single, circular chromosome which is extremely compact and generally has overlapping genes on both strands; no introns, and probably not much alternate splicing of gene products, either, to the best of my knowledge. Bacterial genomes are so small and compact that they simply don’t have room for a lot of non-coding, non-control region junk — rule of thumb is that there is a high selection pressure to keep their own size within certain hard limits, so there is at least that much selection pressure to keep their main chromosome’s size down, too. The difference between the human genome and a bacterial genome isn’t just size; the structural differences and differences in degree of functionality are also immense.

There are also small snippets of independent genetic material passed along through prokaryotic lines as plasmids, which can be (and often are) readily swapped between different species, however. These are not part of the main chromosome, however, and travel independently. It would have been possible — though it looks like it has been controlled for — that mutations which allowed the use of citrate were picked up in plasmids from contaminating bacteria.

@clear_as_mud — “Species” is, as I understand it, an even more nebulous concept when it comes to high-mutation-rate, asexual critters like bacteria; which is why I’ve heard microbiologists refer to “species clouds” of bacteria which are not so much still all the same species, but are still very closely related and not really anything else. You can’t name every single mutated strain a new full taxonomic name, which is why you end up with designations like E. coli O157:H7.

Andrew Conkling
June 5, 2008

Forgive the question, as I’m not a scientist (just a interested dabbler), but I thought that evolution was, in general, a slow process that could not be observed so quickly? Is the situation different for bacteria? Is evolution something that can be observed in a matter of years for them?

Burgy
June 5, 2008

Great experiment. Apologies for the rantings of some of my well-meaning but scientifically illiterate Christian friends.

Over on the ASA list (ASA is an organization of scientists who are also Christians) we have also been commenting on this experiment. ASA may be found at http://www.asa3.org — we have a talk group which anyone may join.

Andrew did read how many generations we are talking about here? 44,000 generations of E. coli since 1988. Human generations we think of around 25 years. Can’t think in terms of human time scales. Evolution is happening all around all the time (not to mention on us and within us). Most of life on this planet isn’t multicellular. Singled celled organisms and viruses are the norm, while we (humans and other multicellular eukaryotes) are the oddity. Look at HIV and drug resistance. Look at the flu. Evolution is very observable over what we humans consider “short” periods of time.

Elf M. Sternberg
June 5, 2008

Bridging a couple of points. At last year’s “Wistar Retrospective”,

Behe decried [Lenski’s] experiments for not doing something they were not designed to do. That is, he noted that none of the E. coli isolates in the experiments have evolved any new structures. He stated his opinion that Lenski’s experiments had shown evidence of parallel gene changes in various populations, but that none of those mutations/deletions occurred in order to benefit the population.

Well, it seems that Lenski’s bacteria have evolved a new structure, one for the consumption of citrate. I wonder if Behe will acknowledge this important challenge to his whole black box theory.

I’m also reminded that at the same conference, pro-ID biologist Ann Gauger discussed an experiment she conducted that did not result in the emergence of the cell structures she anticipated. Reporter Daniel Brooks noted:

She gave what amounted to a second presentation, during which she discussed “leaky growth,” in microbial colonies at high densities, leading to horizontal transfer of genetic information, and announced that under such conditions she had actually found a novel variant that seemed to lead to enhanced colony growth. Gunther Wagner said, “So, a beneficial mutation happened right in your lab?” at which point the moderator halted questioning.

Wagner is a leading professor of evolutionary biology at Yale University.

Andrew: Evolution of bacteria happens constantly since they have several generations per day. This is why we constantly need new and more expensive research into antibiotics: most common bacterial threats have evolved resistance to most of the antibiotics 40 years old, and some (like MRSA) are resistant to almost everything we have today.

Luna_the_cat
June 5, 2008

@Andrew Conkling: we have also observed evolution in
–plants (for example, Spartina anglica, originated as a fertile species as the result of a polyploid mutation around 1870),
–algae (the green alga Chlorella vulgaris made the leap from being a unicellular organism to a multicellular colony organism in the lab, as a random-mutation-strongly-selected-for response to sustained protist predation, around 1988-89),
–insects (for example, the speciation of Culex so-called molestus — there is a taxonomic conflict for that name which has not been resolved, hence the “so-called” — from Culex pipiens, in the 100 years since Culex pipiens followed workers underground as they built the London subway system),
–and mice (a possible 6x speciation of Mus musculus in Madeira over the last 500 years, and a more recent drastic morphological and behavioral change on Gough Island within the last 150 years, although the extent of genetic differences in the Gough Island mice aren’t known yet).

In the normal run of things, we do not observe full speciation events, since full species separation tends to take time. That does not mean that we have not observed evolution leading to speciation, however, or that we have *never* observed speciations. It’s one of those wonderful situations of, now that we have some idea of what to look for and how to look for it, the more we look the more we find.

tinyfrog
June 5, 2008

Nate #31So, I was simply pointing this out that while the bacteria were now able to uptake citrate they were losing other capabilities.

Well, no, you were asserting (without evidence) that this involved the loss of other capabilities. I think it’s clear that you are involved in worldview defense here. You don’t like the idea of useful mutations, so you assert that they have other strongly negative side-effects. I think this is fairly clear from your series of comments. First, you being with some uncertainty:

#22: I would like to know what all the tradeoffs were in these bacteria as well.

Then, later, make an assertion without evidence:

#27: If it is proof for anything is seems fairly obvious that it’s proof that an organism cannot gain a capability through mutations without losing several others.

But back to your comment #31:

I was also simply trying to limit the wrong extrapolations on both sides.

On both sides? No, you’re simply attempting to limit conclusions on the evolutionary side.

Science by definition cannot prove the existance or non-existance of God, whether that God is Jehovah, Ala, or Vishnu.

You’re right about this one. Although many people (including you, apparently) feels the need to undermine scientific results because it’s important to carve out a “science can’t explain it” explanation in order to preserve a place for your God in the universe. Obviously, the evolution of bacteria (or macroevolution, more generally) cannot disprove the existence God, but many theists seem to act like it does and, thus, attack evolutionary evidence as if they are defending God. [sarcasm]I suggest that you widen your attack against all natural explanations, because all of them might erode belief in God. For example, maybe you should complain about the (naturalistic) theory of gravity – which is obviously meant to remove God from the job of pushing us down on the earth’s surface. Attempts to claim that gravity happens naturalistically are obviously attacks on God himself.[/sarcasm] More seriously, you don’t need to undermine evolution or gravity to maintain a belief in God.

Elf M. Sternberg
June 5, 2008

Luna, how could you forget the Mrcaru lizards, as well reported by SB’s own GrrrlScientist? In barely 30 generations the lizard population shifted from an all-insect diet and to a plant-matter-heavy diet, requiring fundamental morphological changes to their gut to acheive that.

But such fundamental changes so quickly show that those lizards already had the potential for such structures in their DNA!

Luna_the_cat
June 5, 2008

Aw, man. You’re right, Elf, I completely dropped the ball on that one.

I guess I got stuck at the mice…..

Torbj�rn Larsson, OM
June 5, 2008

Very interesting article. Maybe we need to conserve the population of bacteria same as we conserve the flora and fauna.

“What is really new about our approach is that we were able to combine both molecular data (DNA sequences) with ecological data in a single mathematical framework,” said Alm. “This allowed us to solve the inverse problem of taking samples of organisms from different environments and figuring out their underlying habitats. In essence, we modeled the evolution of a microbe�s lifestyle over millions of years.”

One splendid example of the difficulty of applying the term “species” to a single-celled creature: 17 of those 25 populations are called V. splendidus, a name that was previously assigned to them based on classical taxonomic techniques. Alm and Polz can see now that V. splendidus has differentiated into several ecological populations.

“Species” is, as I understand it, an even more nebulous concept when it comes to high-mutation-rate, asexual critters like bacteria; which is why I’ve heard microbiologists refer to “species clouds” of bacteria which are not so much still all the same species, but are still very closely related and not really anything else.

Sex in phages is a function of the multiplicity of infection (MOI). When multiple phi6 phages infect the same host cell, they can reassort segments of their genomes.

I interpreted these results as indicative of the purifying selection of sex. Asexual populations are prone to clonal interference, i.e. multiple beneficial alleles compete with each other, but cannot be integrated into the same genotype as sex permits. So, the genetic diversity of the asexual populations remain high, while the sexual populations quickly fix the best available genotype.

Torbj�rn Larsson, OM
June 5, 2008

These are not part of the main chromosome, however, and travel independently. It would have been possible — though it looks like it has been controlled for — that mutations which allowed the use of citrate were picked up in plasmids from contaminating bacteria.

‘Morons’ are genes that bacteriophages carry around which are unnecessary for the virus, but helpful for the host bacteria.

David Marjanović
June 5, 2008

Impressive!

Citrate is […] essentially the same as […] citric acid

It’s exactly the same, depending on the pH: the salts of the citric acid are the citrates.

So, I was simply pointing this out that while the bacteria were now able to uptake citrate they were losing other capabilities.

Not “while”. Long before. Tens of thousands of generations before.

I also don’t see what mechanism you imagine that somehow recognizes a mutation as leading to a “capability” and that somehow destroys “capabilities” to keep their number constant, or something. I recommend an introductory university course into genetics, or for that matter a highschool biology book.

Culex so-called molestus

I thought it’s called C. molestans?

But such fundamental changes so quickly show that those lizards already had the potential for such structures in their DNA!

How do they show that?

David Marjanović
June 5, 2008

It would have been possible — though it looks like it has been controlled for — that mutations which allowed the use of citrate were picked up in plasmids from contaminating bacteria.

The post says they checked for the presence of plasmids and found none.

kenjebz
June 6, 2008

wow
… thnax for this great report.i am a chemist bzsed here in saudi

Luna_the_)cat
June 6, 2008

@David Marjanović — No, I’m pretty sure the fight is over the name molestus. And yeah, on re-reading I am indeed sure they eliminated the possibility that the E. coli had picked up plasmids from anything else.

It is an interesting paper — what I really want to know, though, is what IS the necessary sequence of mutation which preceded Cit+ along that Ara-3 line? What do those mutations do? I would love to know more detail.

Vaughn
June 6, 2008

Thanks to Carl for such a great synopsis of the Lenski long-term lines. I’m a graduate of the Lenski lab and am happy to answer some of the more specific questions about trade-offs. I hope Zachary Blount (the first author on the most recent paper featured on this blog) chimes in to provide a few more specifics.

To summarize, we found that the first few beneficial mutations that took over these populations were pleiotropic , that is, they affected many phenotypes. In some cases, these reduced the ability of the evolved E. coli to grow in other environments. In one notable case, an entire set of genes required for growth on the sugar ribose were deleted. The end results were faster-growing E. coli on glucose, but at the expense of growing elsewhere.

Brian Foote
June 9, 2008

One Major quibble.
You state they controlled for plasmids to make sure the batch was “pure”. There is no nice easy way to check for plasmids unless you check each E. coli cell. Its physically impossible to do the gene sequencing that fast.

Besides their control is stated in the article… They looked at it and if it was cloudy they tossed it. The ol’ eyeball control method isn’t exactly “foolproof”

In this case the scientific facts show that they never had a real control at all except what they could see. On top of this little fact is that it has already been documented elsewhere that E. coli, certain strands, already had the ability to move citrates across its membrane to eat.

Until they do the gene sequencing to actually check for contamination or mutation we are all barking in the wind. If we hear nothing more on this subject the conclusion will be that it was contamination. If they provide a gene sequencing paper that is verified by others, then yes, he probably will get the Nobel Prize. Certainly not until then though.

Brian

jake
June 9, 2008

Ummmmm…….. what is with the Bull crap about this proving evolution? Let me break it down to you. Mutation is the opposite of evolution, meaning it becomes flawed. This whole article is pointless.

Ralph
June 9, 2008

That was a very interesting article.

@Jake:

Mutations are not the opposite of evolution – mutation along with natural selection is what makes up evolution. (From my limited knowledge of biology) A mutation is simply a change in the DNA sequence, and yes, it can be harmful(which most mutations are), and so making the organism “flawed”, or it can be neutral, or beneficial.

Brian Foote
June 10, 2008

Evolution is that lower life forms somehow gain information. Bacteria can “gain info” from bacteria, nothing higher than that.

Once you are above the bacteria stage, then there really is no Mutation that gains information. Mutation of DNA/RNA as a process for gaining information is a dead starting position. It cannibalizes/destroys some information to display its mutation in another direction. For higher life forms you must show how one GAINS INFORMATION. MUTATION NEVER ADDS information it changes what EXISTS. THey never show how such information comes into being in the first place.

Thus, Evolution never gets past the single celled organisms. OF course they have no explanation for how such a cell “appears” in the first place.

In short step 0 no cells they have no explanation
Step 1 1 celled organisms we have some cool bacteria
Step 2 2 celled organisms we have no explanation for higher forms

Step 1×1^nth celled organisms we really have no explanation because everything we do see is decreasing in Genetic complexity, increasing in bad mutations being passed to their children.

Brian

tinyfrog
June 10, 2008

Sorry, Brian Foote, you are making a lot of claims to truth, but they’re only assumptions meant to buttress your own view that evolution can’t work.

Once you are above the bacteria stage, then there really is no Mutation that gains information.
Wait – above the bacterial level, no mutation can add information? So which is it? Mutations can’t produce information (as you claim in your first statement), or mutations can create information in bacteria but not higher organisms? You’re being inconsistent.

Mutation of DNA/RNA as a process for gaining information is a dead starting position.
You need to think more about mutation, probability, and realize that mutations are very capable of (at the very least) optimizing genes. In fact, in order to make the statement that mutations can never produce information, you have to assume that mutations deliberately and mysteriously avoid causing any change that could improve an organism. For example, if a gene has a pre-existing harmful mutation, then you have to claim that all possible mutations to that gene will avoid changing it back to its normal form. You have to claim the absurd position that mutations *know* not to reverse a pre-existing harmful mutation.

craig
June 10, 2008

“Ummmmm…….. what is with the Bull crap about this proving evolution? Let me break it down to you. Mutation is the opposite of evolution, meaning it becomes flawed. This whole article is pointless.”

See, now don’t all you scientists feel foolish? Each of you, having studied for tens of thousands of hours, schooled for years, and thousands of such scientists as you, working for decades… and Jake here is able to destroy all of your work and theories with just a couple of sentences typed between handfuls of cheetos.

kermit
June 10, 2008

Brian@64 “Evolution is that lower life forms somehow gain information. Bacteria can “gain info” from bacteria, nothing higher than that.”

Wow. Where did you get this silly idea? Evolution is a change in alleles in a population over time. There are several mechanisms for this, but the most important is probably natural selection acting on a pool of inheritable variability.

How do you measure information? One common mutation is the duplication of a strand of genetic material. If this happens, another mutation can occur in a duplicate section. How is this not information, by your use of the word?

“Once you are above the bacteria stage, then there really is no Mutation that gains information. Mutation of DNA/RNA as a process for gaining information is a dead starting position. It cannibalizes/destroys some information to display its mutation in another direction.”

No, as I describe in the example above. Don’t you feel better about this conundrum now that you know it was a silly misunderstanding?

“For higher life forms you must show how one GAINS INFORMATION. MUTATION NEVER ADDS information it changes what EXISTS. THey never show how such information comes into being in the first place.”

Well, by mutation. Most mutations are neutral. Some are beneficial, some are harmful. If by higher life forms you mean sexually dimorphic critters like humans, the beneficial mutations tend to spread pretty rapidly. The harmful ones, of course, are those genes which are expressed as traits that are reproductively disadvantageous, and so of course tend to disappear from the gene pool.

“Thus, Evolution never gets past the single celled organisms.”

******************************************************
From: http://www.talkorigins.org/faqs/faq-speciation.html
Boraas (1983) reported the induction of multicellularity in a strain of Chlorella pyrenoidosa (since reclassified as C. vulgaris) by predation. He was growing the unicellular green alga in the first stage of a two stage continuous culture system as for food for a flagellate predator, Ochromonas sp., that was growing in the second stage. Due to the failure of a pump, flagellates washed back into the first stage. Within five days a colonial form of the Chlorella appeared. It rapidly came to dominate the culture. The colony size ranged from 4 cells to 32 cells. Eventually it stabilized at 8 cells. This colonial form has persisted in culture for about a decade. The new form has been keyed out using a number of algal taxonomic keys. They key out now as being in the genus Coelosphaerium, which is in a different family from Chlorella.
*****************************************************

So a single-celled organism adapted to a threat by becoming a colony organism (the simplest of multi-celled).

“Of course they have no explanation for how such a cell “appears” in the first place.”

Irrelevant to how evolution worked to produce the diversity of life, after the first cells showed up. There are folks who are doing serious work on how abiogenesis happened. We’ll get back to y’all when we get it figured out.

“In short step 0 no cells they have no explanation”

Sometimes the answer is ‘we don’t know’.

“Step 1 1 celled organisms we have some cool bacteria
Step 2 2 celled organisms we have no explanation for higher forms”

Sure we do. I showed you how a first step to multi-celled life was observed just a few years ago.

“Step 1×1^nth celled organisms we really have no explanation because everything we do see is decreasing in Genetic complexity, increasing in bad mutations being passed to their children.”

You are seriously confused, lad. We have a very good understanding of how recent evolution occurred. (Which doesn’t mean we don’t have a lot more yet to learn.) Mutation is a change in the genes passed on to the next generation; most mutations are neutral. You have about 100 mutations yourself, as do I. Bad mutations (genes expressed in reproductively disadvantageous ways) do not get passed on very well. Why on Earth would harmful genes accumulate?

And what *do you mean by “information” in this context?

clear as mud
June 11, 2008

OMG, this is still hopping here.

I see the two biggest anti-evolution lies are active.
1) “Mutations are all bad, evolution can’t use it”
2) “Nothing in the universe confers “INFORMATION ™” to help evolution. No don’t ask me what “INFORMATION ™” means! I haven’t thought it through enough!”

thus, all of science is wrong.

Another annoying tendency by these folks:
1)Demand a complete explanation of every minute event from the beginning of time to today, whether or not enough research has ever happened.
2)Deny every point, anyway, because you don’t believe anything scientists say.
3)If there is even the tiniest uncertainty, though, it absolutely proves all of science is LYING!

(Man, life is so easy this way… you’re right no matter how wrong you really are!)

Brian Foote
June 11, 2008

You keep saying some mutations are good bad indifferent. whether that statement is right has no bearing on the discussion. You can’t get DNA from NO DNA its blatant ignorance to say otherwise.

For a single cell to exist it must
1) have a cell wall
2) Ways to pass food/waste through cell wall
3) Digest said food
4) Differentiate Between what is good and waste to get rid of waste
5) Replicate itself.

If any of the above do not exist all at the same time you never get to single celled organisms.

Evolutionists still have the problem that once said cell with its 400 genes(simplest single celled organism we know of) exists it has to gain more genes. Mutations don’t add Genes to DNA strands. They change what is there. Changing of 400 gene DNA strands trillions of times won’t make DNA strands with 401 genes. There is no process to INCREASE the amount of information inherent in the single celled organisms.

Fact is, for people to believe evolution you must show the steps otherwise you are simply believing that evolution is true.

Fact, evolutionists believe by faith that the universe spontaneously appeared with no scientific supporting evidence and plenty against it.

Fact, evolutionists believe by faith that a single celled organism spontaneously appeared.

Fact, Evolution is Faith

Brian

chrisD
June 11, 2008

Brian, you are a right moron. I won’t even touch the other things you mentioned because they are irrelevant. But you should know better than to equate abiogenesis with evolution. Unless you skipped that section of the pamphlet they were handing out in Sunday School.

This renders your point of evolution requiring faith moot and unfounded since evolution does not entail what you claim it does.

Brian Foote
June 11, 2008

I notice you never even bothered to answer my DNA point for increasing DNA strand length, just started name calling… Still waiting for a rational explanation of that one…

Did you even read what you wrote ChrisD? Abiogenesis is the base of evolution and those who want to claim there is no God.

Did you miss the simple logic card passed out at the latest atheist rally?

Step 1 life came from non life? Followed by Step 2 life obtaining more complex DNA somehow…

Brian

Owlmirror
June 11, 2008

Evolutionists still have the problem that once said cell with its 400 genes(simplest single celled organism we know of) exists it has to gain more genes. Mutations don’t add Genes to DNA strands. They change what is there. Changing of 400 gene DNA strands trillions of times won’t make DNA strands with 401 genes.

Actually, gene duplication is a common mutation. They are not quite as common as point mutations, which is what you’re babbling on about, but they do happen.

[Mutations don’t add Genes to DNA strands. They change what is there. Changing of 400 gene DNA strands trillions of times won’t make DNA strands with 401 genes. There is no process to INCREASE the amount of information inherent in the single celled organisms.]

Can you prove that with 100% certainty? I don’t think so. I know there has been at least 1 documented case of genetic mutation which has fused 2 genes into 1 in the human genome (via researching using alleles on said gene which were found not only at the ends, but also in the middle). Why would it be impossible for a mutation to not create an extra? Improbable? Perhaps. Impossible? No. It may have already happened and just not been a beneficial mutation that was passed along.

Owlmirror
June 11, 2008

You can’t get DNA from NO DNA its blatant ignorance to say otherwise.

No, it follows as an inference from biochemistry. We are ignorant of the process, but no one — certainly not a ignoranimus like you — has ever shown as a biochemical fact that it is impossible.

To do so, you would need to examine every single organic chemical compound and combination of compounds, in every possible environment, exposed to every possible combination of energy inputs.

You, on the other hand, would have trouble adding vinegar to baking soda unsupervised.

Fact, cosmologists believe the evidence that the universe spontaneously appeared, with plenty of scientific supporting evidence and no coherent argument against it.

Fixed.

Fact, evolutionists infer from the evidence that a single celled organism eventually developed from some combination of complex chemical replicators and/or complex metabolic-like chemical reactions, possibly by way of some additional catalyst.

Fixed.

Fact, Evolution is a theory and a fact.

Fixed.

Pop
June 11, 2008

Creationsits should understand that the writing by various personages from biblical times were more reporters of the news of the time, while science tries to give a step-by-step of how things seem to go together and work. A sort of book of direction on how to fix things.

I see no great divide between belief in God and accepting the information of how provided by science. It all fits rather nicely. Because a thing is not explained in the Bible does not prevent it from being or happening.

chrisD
June 12, 2008

I notice you never even bothered to answer my DNA point for increasing DNA strand length, just started name calling… Still waiting for a rational explanation of that one…

Did you even read what you wrote ChrisD? Abiogenesis is the base of evolution and those who want to claim there is no God.

Well if you don’t want to be called names then quit fitting the definition of those names so well. How can I argue with you since what you are saying with regard is wrong on a factual level as it relates to evolution?

Evolution has nothing to say about the origin of life, but states that once the ball got rolling (in whichever method suits your emotions best), evolution by natural selection is what lead to the diversity we see today. Period. No speculation about which unmoved mover diddled what diddley where to get the ball rolling – it’s irrelevant.

Brian: Usually we talk about mutations as if they were simple “letter” changes. This –> Thus —> Thug etc. Sometimes the machinery that duplicates DNA screws up; sometimes some outside “insult” damages the DNA (radiation, or a chemical). If that were the only way mutations arose, it would make sense that the number of genes wouldn’t change. But as the pharyingula link points out, the machinery that duplicates DNA can screw up in other ways too. Sometimes when it’s copying DNA, it copies the same part twice. This gives two identical copies of a stretch of DNA. If there were genes in that stretch, now there are two copies of each one. Often, that can be a harmful thing: some proteins have to be in a cell at specific levels, and if there’s two copies of a gene creating a protein, that can be bad. On the other hand, sometimes there’s a lot of flexibility built in to the system, and a cell can cope with this.

With two copies, a cell gains a certain “freedom.” If you owned one car, you might be reluctant to tinker with it, since it’s the only car you have. With a second car, you might feel more free to “pimp” one car a bit, since now you have a spare if you somehow damage the first car beyond repair. In my example, of course, there’s a conscious decision involved. In the case of cells, this simply means that a cell doesn’t *care* what happens to the extra copy of the gene. Sometimes it acquires a harmful mutation. Cells can usually safely ignore this, now, since they never needed that copy of the gene in the first place. Indeed, the human genome is littered with examples of “pseuodgenes” which no longer do anything, but which seem to have arisen as copies of genes which DO have functions. But sometimes, this tinkering creates something new. It doesn’t even take a LOT of tinkering. In Owlmirror’s example, a gene whose product helps detects light duplicated, and then changed so that it was senstitive to a different color of light. In this way, you can go from “black-and-white” light sensitivity to color vision (I know, I’m simplifying a bit). There’s a ton of other examples of a duplicated copy of a gene being altered to have a new function. In biology, we often talk about “gene families” in which a single gene was duplicated over and over until you have sometimes dozens of related genes which all do different things. Often, you can identify these duplicate genes because they’re located near the original gene (in one species you find a single copy; in another species you find two), though over time, genes can shuffle themselves around.

The point in all of this, though is that even if you start with 400 genes, there are a number of mechanisms for increasing the number of genes over time.

Zachary
June 12, 2008

Hi, my name is Zachary Blount. I am the first author on the paper this posting describes. I am sorry I am late coming to the party here, but I was traveling when it came out, and just now got home to regular internet access. If anyone is still checking this comment section, I would be happy to answer in as timely a fashion as I can anyone’s questions that would help clarify the research described in the paper.

Larry Fafarman
June 12, 2008

Zachary Blount said,

I am the first author on the paper this posting describes. I am sorry I am late coming to the party here . . . . If anyone is still checking this comment section, I would be happy to answer in as timely a fashion as I can anyone’s questions that would help clarify the research described in the paper.

There is not just this comment section — hundreds of comments about your research are on the New Scientist magazine website, the Panda’s Thumb blog, the Uncommon Descent Blog, Ed Brayton’s Dispatches from the Culture Wars blog, and possibly other places. Michael Behe wrote a response to your research results. Links to these websites (except Ed Brayton’s blog) are on my following blog post:

BTW, all of the blogs mentioned except mine practice arbitrary censorship of comments and commenters and so may be unreliable.

The following comment is excerpted from the above post on my blog:

The mutations appear to have occurred at two or even three stages — the first — or preliminary — mutation at around the 27,000th generation (around the 20,000th generation according to some sources), the second at around the 31,500th generation, and possibly a third around the 33,000th generation.

Question: To what extent did the first mutation spread through the population, if it spread at all, considering that it apparently conferred no advantage?

There were around 44,000 generations in 20 years, or about 2,200 generations per year. So assuming that the first mutation occurred at 27,000 generations and the second occurred at 31,500 generations, that would be about 2 years from the first mutation until the second mutation. That seems to mean that the second mutation is rare — however, on the other hand this second mutation appears to be common because it was repeated numerous times by starting with the unfrozen samples of previous generations. So how could the second mutation be both rare and common at the same time? Maybe the second mutation is really quite common but is rarely expressed because there are relatively few individuals with the first mutation, which confers no advantage.

Carl Zimmer says in the original post,

Blount took on the job of figuring out what happened. He first tried to figure out when it happened. He went back through the ancestral stocks to see if they included any citrate-eaters. For the first 31,000 generations, he could find none. Then, in generation 31,500, they made up 0.5% of the population. Their population rose to 19% in the next 1000 generations, but then they nearly vanished at generation 33,000. But in the next 120 generations or so, the citrate-eaters went berserk, coming to dominate the population.

The original post gives the following explanation for the preceding observations:

This rise and fall and rise suggests that the evolution of citrate-eating was not a one-mutation affair. The first mutation (or mutations) allowed the bacteria to eat citrate, but they were outcompeted by some glucose-eating mutants that still had the upper hand. Only after they mutated further did their citrate-eating become a recipe for success.

Actually, the rise and fall at 31,500 and 33,000 generations respectively is not what indicates that the citrate-eating trait is not just a one-mutation affair, because — as noted above — it appears that an essential preliminary mutation occurred at around 27,000 generations (around 20,000 according to some sources).

Also, in a sense the citrate-eating bacteria are not really competing with the glucose-eating bacteria, because the two kinds of bacteria have different food sources.

The citrate-eaters were initially getting quite good at competing with the glucose-eaters, rising to 19% before nearly vanishing and then becoming dominant. The opening post does not adequately explain why the citrate-eaters nearly vanished.

Also, the original post said,

Lenski started off with a single microbe. It divided a few times into identical clones, from which Lenski started 12 colonies. He kept each of these 12 lines in its own flask. Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. And on and on and on, for 20 years and running.

As I calculated above, there is an average of about 2,200 generations per year, so if a new population was started each day with a sample from an old population, then there were about 6 generations per population. With only 6 generations, there might be a significant possibility — depending on the size of the sample — that a mutation occurring in an old population would not be collected in the sample used to start the next population, particularly if the mutation occurred in one of the last generations of the old population. The populations should of course be well-stirred before collecting the samples to start the next populations — the original post says that he flasks full of E. coli were placed on a “gently rocking table”, and I presume that means that the populations were well-stirred before collecting the samples.

I think the results fit a lot more easily into the viewpoint of The Edge of Evolution. One of the major points of the book was that if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it. But if more than one is needed, the probability of getting all the right ones grows exponentially worse. “If two mutations have to occur before there is a net beneficial effect — if an intermediate state is harmful, or less fit than the starting state — then there is already a big evolutionary problem.” (4) And what if more than two are needed? The task quickly gets out of reach of random mutation.

I agree with Behe. Even though I think that the second mutation in the Lenski-Blount-Borland study is fairly common (because it often re-appeared in populations that descended from frozen samples of the 27,000th — or 20,000th according to some sources — generation or later), it took approx. 4,500-11,500 generations or approx. 2-5 years for the second mutation to be expressed at approx. the 31,500th generation, and I think that was because there was a scarcity of bacteria with the preliminary first mutation because the preliminary first mutation alone conferred no advantage in survival. So if more mutations are needed, the chance of getting all the right ones in one bacterium grows exponentially worse, as Behe said.

I wonder if there is any data on how quickly the second mutation was re-expressed in the populations descended from the unfrozen populations of 20,000-27,000 generations or later.

Jennifer Rodriguez-Mueller
June 13, 2008

I know I’m days late to the party but I just wanted to chime in to direct people’s attention to a really cool and conceptually related paper on the evolutionary robustness of genetic coding schemes:

(
Bacteriophages are viruses that eat microbes and there’s ~10 of them for every bacteria on the planet and they’re a huge driver behind evolution. Everyday, bacteriophage kill in the ballpark of a third of the bacteria on the planet. They can steal genes from their hosts, mess around with them for their own ends for generations, and insert them into other hosts. This makes them (1) potential generators of genetic novelty, (2) potential mechanisms for lateral gene transfer (like plasmids, which keep being brought up) and (3) predators of bacteria that can potentially drive bacterial evolution through red queen dynamics. If you want to maximize the number of “independently selectable copies” of a protein that might jump around and mutate in crazy ways, bacteriophage aren’t a bad place to look.
)

Anyway, the article I wanted to direct people’s attention to gets quantitative with bacteriophage evolutionary issues in a cool way:

=====ABSTRACT START======
A compensatory mutation occurs when the fitness loss caused by one mutation is remedied by its epistatic interaction with a second mutation at a different site in the genome. This poorly understood biological phenomenon has important implications, not only for the evolutionary consequences of mutation, but also for the genetic complexity of adaptation. We have carried out the first direct experimental measurement of the average rate of compensatory mutation. An arbitrary selection of 21 missense substitutions with deleterious effects on fitness was introduced by site-directed mutagenesis into the bacteriophage {phi}X174. For each deleterious mutation, we evolved 8 – 16 replicate populations to determine the frequency at which a compensatory mutation, instead of the back mutation, was acquired to recover fitness. The overall frequency of compensatory mutation was ~70%. Deleterious mutations that were more severe were significantly more likely to be compensated for. Furthermore, experimental reversion of deleterious mutations revealed that compensatory mutations have deleterious effects in a wild-type background. A large diversity of intragenic compensatory mutations was identified from sequencing fitness-recovering genotypes. Subsequent analyses of intragenic mutation diversity revealed a significant degree of clustering around the deleterious mutation in the linear sequence and also within folded protein structures. Moreover, a likelihood analysis of mutation diversity predicts that, on average, a deleterious mutation can be compensated by about nine different intragenic compensatory mutations. We estimate that about half of all compensatory mutations are located extragenically in this organism.
======ABSTRACT END=======

Basically it’s good to remember that the longer the descendants of a single isolated strain “hang out” the more chances for harmful mutations that are subsequently compensated for. It’s likely that over time, you’ll get a “halo” of genomes with genetic differences (with different potentials for positive mutations) that are nonetheless reasonably stable as far as gross phenotype goes. And the bigger the disaster the better chance there’s a way to compensate for it…

A lot of quantitative/theoretical issues with “multiple steps to find a positive mutation” are ameliorated when you remember this. Genomes might be simply that robust. Instead of “two improbable steps” it might be more plausible to imagine “twenty damage/repair cycles that eventually open up a new path”.

—

It would be keen to see if different prophages (bacteriophages laying dormant in a bacterial genome) are lurking in any of the involved strains.

A lot of times they pop out just by exposing a culture to bit of DNA damage (the phages detect the DNA damage and you get a “rats fleeing a sinking ship” effect as bacteria start to die from viruses) so it’d be cheap to try for a clear positive sign that phages might be involved before going to the trouble of sequencing anything. If the phages pop out you could sequence just the phages, rather than the whole genome. Bacteriophage genomes are frequently less than a hundred kilobases.

(Apologies if some of the bacteria have already been sequenced or otherwise checked for phages, I couldn’t get the full paper because I don’t have academic library access right now.)

Greg Laden
June 13, 2008

Larry F: Why would you not assume that a given mutation can spread even though it does not confer an advantage? A mutation can be neutral, and thus, the chance of a given mutation spreading is in some ways like the chance of someone winning the lottery. It happens every time they run a lottery that someone wins! (But you and I are not going to). This is basic probability.

Boomer
June 13, 2008

Just to add to what Greg said, neutral mutations actually have a very good chance of spreading through the gene pool. This mechanism is called genetic drift and is especially probable in small populations such as these.

Stephanie Z
June 13, 2008

Thank you, Larry. I’ve been really puzzled by the basic concepts behind some ID lines of thought, but your comment made one of them absurdly clear.

Who (besides Behe) suggested that only mutations that confer a direct advantage get passed on? In fact, the only mutations that are likely not to get passed on are the radically nonadaptive–the rapidly fatal ones, those that prevent reproduction, etc. Everything else, barring accident or unfitness unrelated to the mutation, will get around a bit. I mean, really, if the tendency to store fat in such a way as to create a beer belly is still with us….

Greg Laden
June 13, 2008

I think part of the confusion is the conflation that happens all the time among creationists between day to day population genetics and selection.

Try it. Recite this mantra several times a day for several days:

“Evolution is not real. It is not possible to achieve the complexity we see in life from mere random chance. An aardvark cannot be assembled when the tornado hits the junkyard.”

After a while you will conflate selection and mutation as one process. That can lead to the benighted confusion we see above (and generally in everything Larry F. writes or says. And Behe.)

factician
June 13, 2008

Stephanie,

My beer belly isn’t adaptive? What about as a source of energy to keep me warm in winter?

I’m not a biologist, so forgive me if this sounds ignorant. Will the evolved E. coli be sequenced so that the actual gene changes can be located? Also, the other populations which did not evolve this capability, would they also be sequenced to find if they carried a neutral change? I’m just ecstatic about this research, it is cool beyond cool.

Boosterz
June 13, 2008

Who left the door open on Larry’s cage? How many times do I have to say it, when you get done poking him with the stick, MAKE SURE TO CLOSE AND LOCK THE DOOR!

firemancarl
June 13, 2008

Arguing with Larry is as smashing your head into a brick wall. Don’t worry folks. As Larry the Omnipotent told us on the Florida Citizens for Science webpage If he wasn’t taught it in high school (1960s) then it is not valid!

Marcus Ranum
June 13, 2008

What are the ODDS against that happening!!
Goddidit!

Just kidding.

raven
June 13, 2008

Just skimmed this thread and am a bit time pressed today.

Lots of questions about this paper. For the cognescienti, if they will.

1. IIRC, Lenski et al. found 1/3 of their lines picked up mutator phenotypes. Are these the ones that evolved cit+?

2. What do you/they think of the various adaptive mutation theories which have some experimental support floating around. e.g. the work of Hall, BG and so on?

3. The cit+ cultures seem to require 3 mutations. I realize the nature of all 3 probably aren’t known, but what info do you have? One of my wild guesses would be a mutator, followed by a permease specificity change, and maybe upregulation of the permease and/or the enzymes that metabolize citrate, the TCA cycle. TIA.

Roger Garcia-Marenco
June 13, 2008

Awesome, fascinant, overwhelming to say the minimum, the educative power of it is beyond imagination and I wonder if to raise the collective knowledge and wisdom of our species
a similar endevour could be run with entities we use to call “creationists” in order to explore the possibilities that our species could ever become, collectively, scientifically aware of itself and its surroundings in logical and rational terms and so left behind the misleading viral concept of God that unfortunately long ago Plato set up so absurdly but disguised as logical.

Moses
June 13, 2008

Who left the door open on Larry’s cage? How many times do I have to say it, when you get done poking him with the stick, MAKE SURE TO CLOSE AND LOCK THE DOOR!

Posted by: Boosterz | June 13, 2008 11:49 AM

I love Larry. He, with his bizarrely ill-informed opinions on law, biology, history and, well, pretty much everything encapsulates our narcissistic, self-important Country’s mind-set better than any textbook could ever hope to achieve.

Plus, Larry has a rock-solid function in life. I equate Larry to the South Pole of a magnet, wherever he points, you can find the truth in the opposite direction.

Drew
June 13, 2008

Raven I was also trying to think about the nature of the mutations specifically why the cit+ mutation was so rare. What was that first mutation that seems to have made the whole thing possible so rare. I also have a wild guess of a duplication event. That quite possibly and quite randomly the gene for an existing necessary transmembrane transporter was duplicated and then later mutated to transport citrate.

Here’s why I thought of this, if the gene was necessary then the mutation could have happened in other strains but the mutants wouldn’t be able to survive. The duplication would be a pretty rare event, and once that happened there would be a copy that could mutate freely.

Of course I’m pulling all of this from the ether as they say, or used to at least, and could be and probably am entirely wrong. But it’s fun to think about and conjecture on when I know that I’m not the one that has to do the work

mcmillan
June 13, 2008

Raven,
My understanding of the paper was that this wasn’t in the strains with the mutator phenotype, but a specific mutation for citrate transport.

I’d also be curious what is known about the nature of these mutations. I was thinking the same hypothesis as Drew. It seems prettly plausible that this was duplicating some other membrane channel or transporter which then needed further mutations to have efficient specificity for citrate.

I should probably just ignore the trolls, but I do have a question for those that are arguing that mutations can only result in the loss of information. If some mutation, let’s say at T->C, results in a loss of information, how is it prevented from going C->T again since gaining information is supposedly impossible?

Mike Haubrich, FCD
June 13, 2008

There must be a need among those who think evolution is cool and want to learn more (like by reading Carl’s books) to respond and try to educate the willfully ingorant such as Brian Foote and Larry Fafarman.

They don’t care about the facts of evolution and how the process of discovering those fats work. The intent is to get attention and that’s why they troll. They are hungrgy for argument, not for knowledge. This is why the sign says “Don’t feed the trolls.”

Ignore them. They go away. Trust me on this.

James Walden
June 13, 2008

I love the idea of being able to restart evolution outside of a computer simulation. However, how do you control for the effect of freezing and thawing the bacteria? Do any of the bacteria die or suffer genetic or somatic damage that would cause them to be different?

Rosie Redfield
June 13, 2008

Hey Zachary, why did Rich have citrate in the medium when he started the lines? I don’t think it’s a standard component of minimal media for E. coli.

Rev. BigDumbChimp
June 13, 2008

Stephanie,

My beer belly isn’t adaptive? What about as a source of energy to keep me warm in winter?

*sigh*

Fuel tank for the love machine.

noncarborundum
June 13, 2008

I know there has been at least 1 documented case of genetic mutation which has fused 2 genes into 1 in the human genome (via researching using alleles on said gene which were found not only at the ends, but also in the middle).

Kahlan, are you sure you’re talking about genes? Genes don’t have alleles on them; different version of the same gene are alleles. I rather suspect you’re really referring to the human chromosome 2, which looks like a fusion of chimpanzee chromosomes 2p and 2q. Among other evidence, the middle of human chromosome 2 has a region of telomeric DNA, which is normally found at the ends of chromosomes.

A fusion of chomosomes doesn’t need to change the gene number. But gene duplication, which does, is amply documented.

David Marjanović
June 13, 2008

I should probably just ignore the trolls, but I do have a question for those that are arguing that mutations can only result in the loss of information. If some mutation, let’s say at T->C, results in a loss of information, how is it prevented from going C->T again since gaining information is supposedly impossible?

You act as if those people knew what A, C, G and T are.

Do any of the bacteria die or suffer genetic or somatic damage that would cause them to be different?

In a word, no. Freezing & thawing, if done right, are completely harmless.

>This is total horse crap. There’s nothing in the Bible to suggest >that evolution exists. You’re just arbitrarily making up excuses.

Are you for real??

>If the bacteria changed, it was clearly because God willed it. He >does that sometimes, you know.

Ah,yes. But the researchers held a Black Mass over the flasks twice a day so God couldn’t get near enough to do that. [ Wonder how they managed to dump all the bodies of the babies they sacrificed?]

>Just because God helped the bacteria survived, you can’t just simply >say it’s because we come from monkeys. That’s stupid and arrogant.

You may come from a monkey. Inspect your coccyx to see if you have a prehensile tail attached. I, on the other hand, evolved from an ape that evolved from a lemur, that evolved from a small rodent-like mammal………

>You’ll go to hell for your blasphemy.

Thank goodness. ‘Cos all the loonies like you will be in heaven which will make that a really bad place to be for a day, never mind eternity.

factician
June 13, 2008

Raven,

Mutators happen in environments that are highly selective. When people sequence mismatch repair (mmr) genes from pathogens, they find that the mismatch repair genes are more divergent from each other than control genes in the rest of the population, as if the cells have mutated to mismatch repair minus over short periods of time, and then mutated back to mmr+. This is from work done by Miro Radman about 8 years ago that has been shown over and over since then. So seeing mmr- in an environment like the Lenski experiment isn’t all that surprising.

David,

Freezing and thawing E. coli cultures results in small losses of viability. If you’re just looking for viable cells, you’ll almost always find them. But if you look at the number of cells in the frozen sample, it will decrease with each freeze/thaw cycle. That said, you’re right, of course, that there wouldn’t be expected to be any changes in the genetic content of said cells.

Marcus Ranum
June 13, 2008

Everyday, bacteriophage kill in the ballpark of a third of the bacteria on the planet. They can steal genes from their hosts, mess around with them for their own ends for generations, and insert them into other hosts.

But they’re not creating INFORMATION that way! They’re just, uh.. Sorry, I just laughed soda out my nose.

Richard Wolford
June 13, 2008

“Information”. The creotards keep using that word. I do not think it means what they think it means.

clear as mud
June 13, 2008

Richard #109: I wrote a post about that. It only addresses the “information” issue from one minor perspective, though. Heck, you could write like 20 essays to address all the possible meanings of creationists’ “informayshunz”

noncarborundum
June 13, 2008

noncarborundum, you can’t omit the http part.

Do tell.

David Marjanović
June 13, 2008

Are you for real??

I think the whole comment was a parody. Poe’s Law prevents me from finding out, though.

noncarborundum
June 13, 2008

>Posted by: Ken Finley Comment #21

>This is total horse crap. There’s nothing in the Bible to suggest >that evolution exists. You’re just arbitrarily making up excuses.

Are you for real??

One never knows, does one? I first read this as entirely serious, but now I’m not so sure.

Speaking of which, I just discovered there’s also a Christian evangelical principle called “Poe’s Law”:

“Poe’s Law” is a Christian theological principle that states: “Elements of the Gospel speak to different levels of spiritual concern in different cultures at different times.” It is taught to modern evangelists as a way to better target the message of the Gospel to different audiences for maximum salvific efficacy. The law was named after theologian Dr. Harry Lee Poe, a cousin of Edgar Allan Poe, who promoted the concept in his book “The Gospel and Its Meaning: A Theology for Evangelism and Church Growth.” (Urban Dictionary)

Oh to have maximum salvific efficacy now that Spring is here.

Nicole
June 13, 2008

@Zachary

No question, just bravo on the fabulous research!

Zachary
June 13, 2008

Hello everyone!

I apologize for not getting to answering questions as quickly as I had hoped. As I said earlier, I just got back from attending a conference, and realized last night the one I will be attending late next week is, well, next week, and that I have a goodly number of things to prepare for it. Carl suggested writing a general post addressing various questions and clarifying the research a bit. I hope to have this together and to Carl next week. If you have anything you would like to see addressed (no guarantees), please post either here of one of the more recent posts Carl has made on our paper. In the meantime, I think everyone who interested and has questions should definitely read the paper itself, and Carl has been kind enough to link to the pdf of it on Dr. Lenski’s webpage. The paper goes into great detail on the research and how we did what we did. It is a good place to start. If, after reading it, you are still puzzled, please post here, and I will see what I can do to help you out. I hope everyone finds the phenomenon I study as incredibly nifty and interesting as I do, and I want people to understand it (to the extent that it is currently understood – there are many unresolved questions, as there always are in science at any given time – give me a few decades to work, and I promise I will answer a good many of them!).
I would also direct people to Dr. Lenski’s webpage (https://www.msu.edu/user/lenski/) publication list because a great many papers dealing with the long term evolution experiment and associated research are present there in pdf format. Those not there may be found in most any academic library, and, even if you are not a student at the associated institution, most are willing to allow the public to examine their journal holdings. As always with science, there is much that has to be left out in popular accounts of research, and you should always when possible go to the original reports in peer-reviewed journals. The reading can be difficult, but quite rewarding. For our work, I would suggest that you start with a detailed review of the long term experiment and the findings to have emerged from it that Dr. Lenski wrote a couple of years ago. It is publication #147 in the complete list (“Phenotypic and genomic evolution during a 20,000-generation experiment with the bacterium Escherichia coli”). The list includes a large range of peer-reviewed research dealing with many issues, including beneficial mutations and how we study them, mutation supply, adaptive dynamics, the pace of evolution, crossfeeding interactions (when one group of bacteria in the population produce a substance that other bacteria in the population can then use), and even indications of incipient speciation in one of the other twelve populations.
I would, however, like to address the issue of the citrate in the medium. I have seen a number of references here and on other blog comment sections calling the citrate in the medium a “control”. I am a bit unclear as to where this is coming from. The citrate is not included in the medium as a control. We do have a control flask called a blank that is always included when we transfer the twelve populations. This blank included only the DM25 liquid medium in which the populations grow. It is just ten milliliters of medium that we don’t put bacteria into during transfers. This allows us to know if the medium is contaminated. I think there was some confusion of the citrate in the medium with this blank. So, what is the citrate doing there? Well, it is part of the DM25 recipe, and has been since it was first reported by Bernard Davis and Elizabeth Mingioli in 1950 (Davis and Mingioli 1950. Mutants of Escherichia coli requiring methionine or vitamin B12. Journal of Bacteriology 60(1): 17 – 28.). They included it for two reasons. First, E. coli use something called the ferric di-citrate iron acquisition system to take up iron from their environment, though in this system, the citrate never enters the cell (see Hussein, S., Hantke, K., and Braun, V. 1981. Citrate-dependent iron transport system in Escherichia coli K-12. European Journal of Biochemistry, 117: 431 � 437.). While E. coli have another set of genes for what are called enterochelins, which can also be used for iron acquisition, citrate is commonly included in defined E. coli growth media (defined media are growth media for which we known exactly what is there and in what amount, as opposed to rich media such as Luria broth, trypticase soy broth, or brain heart infusion, which include enzymatic digests of yeasts and various proteins and, yes in the case of the third one, brains and hearts of cows which can vary in their exact constituents) just to make sure that the bacteria don’t starve for iron. Also, when the media from which DM25 was developed were first formulated in the early to mid-20th century, it was common to keep them in 50x stocks that were then later diluted with water before use. At this concentration, the sodium citrate concentration was increased beyond what the organism strictly needed to prevent another component of the medium, magnesium sulfate, from precipitating out. As E. coli were not bothered by this, no other thought was given to the issue. I find this rather interesting, as it means that the citrate concentration in DM25 is also something of a matter of historical contingency – the niche for the Cit+ variant E. coli I study would not be nearly as large had not those bacteriologists of long ago not been so concerned about saving space! I would need to check with Dr. Lenski as to precisely why he chose DM25, but I am pretty sure it was a medium he had worked with before. Certainly he saw the glucose level as more important, and it is very easy and non-troublesome to alter the amount of glucose in DM25. The principal questions of the long term evolution experiment may be found in the publication #147 I mentioned above in section A, “Motivating Questions”. One of the most significant draws from Gould. As the ancestor of the twelve populations was a single cell, they started off as genetically the same (save for a single marker trait that involves a difference of single nucleotide). As such, the experiment is like playing the same tape of life, twelve times simultaneously. From this came the question: if these are the same tapes, evolving in identical environments under identical conditions, how parallel or divergent will be their evolution? The papers listed on Dr. Lenski’s webpage will show that much work has been done into this. When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding – I will need to check with him to make certain I understand this properly). However, and unsurprisingly given that there has been only one report of a spontaneous Cit+ mutant of E. coli in the past century (Hall, B. 1982. Chromosomal mutation for citrate utilization by Escherichia coli K-12. Journal of Bacteriology, 151: 269 � 273.), none did (which wasn’t a problem – despite some misunderstanding on the internet, the intent of the experiment was never to evolve a Cit+ E. coli variant)…until, after 31,000 generations of evolution and fourteen years of the experiment, one population we call Ara-3 figured it out. It is with this that the paper deals, and my ongoing work is to figure out how this novel innovation evolved, its genetic basis, the underlying physiology, the resulting ecological interactions between the co-persisting Cit+ and Cit- variants and how they change over time as the variants evolve, and the long-term evolutionary consequences for the population, as well as developing it as a model system for the examination of interesting evolutionary questions. There are some details on these future directions in the paper’s discussion section, and I suggest you read it if you are interested. In short, there is much to be done, and Dr. Lenski and I hope to provide you with interesting reading material for a long time to come.
I hope this answers the citrate question, and perhaps a few other. As I said, I hope to have a general post ready next week.

Thank you,
Zachary

PS For those interested, the tower which the time lapse video shows was composed on 13,704 petri dishes that accumulated through experiments performed from October of 2006 to November of 2007 (the total number of plates used in the research described in the paper was around 20,000 – all courtesy of our lab manager and her assistant). I think I saw a comment somewhere that seemed to indicate that the tower was itself part of the experiment. It was not. When and experiment was finished, I was done with the plates, and I put them in the cold room for storage. This started a few years ago as just a fun exercise to see how much medium I was using. I ended up deciding to save plates between my yearly progress report meetings with my research advisory committee, and then building a tower so I could have a slide in my presentations to the committee allowing me to assert that my data were based on real work (which wasn’t in doubt, but a good slide is a good slide). Besides, I used to build structures of stacked rock just for fun when I was growing up, and stacking petri plates is not terribly far removed. Not as permanent (or odorless), but just as much artistic fun. Science and art are not mutually exclusive endeavors, after all.

Sili
June 13, 2008

I just want to say thank you to Zachary for taking the time to answer questions – and to him and his coworkers for designing such a nifty experiment.

And Dr Zimmer’s summary was excellent – even this interested layman felt enlightned.

Larry Fafarman
June 13, 2008

Greg Laden said (June 13, 2008 10:43 AM) —

Larry F: Why would you not assume that a given mutation can spread even though it does not confer an advantage?

The bacteria possessing only the first mutation would be as likely to starve as the other bacteria that can eat only glucose. Anyway, providing an advantage greatly increases the rate of a mutation’s spread. I thought that was the whole idea behind the principle of natural selection.

Boomer said (June 13, 2008 11:07 AM) —

Just to add to what Greg said, neutral mutations actually have a very good chance of spreading through the gene pool. This mechanism is called genetic drift and is especially probable in small populations such as these.

These populations are not small — they consist of millions — maybe even billions — of bacteria.

Stephanie Z said (June 13, 2008 11:08 AM) —

Thank you, Larry. I’ve been really puzzled by the basic concepts behind some ID lines of thought, but your comment made one of them absurdly clear.

Who (besides Behe) suggested that only mutations that confer a direct advantage get passed on?

Neither Behe nor I suggested that.

raven said (June 13, 2008 12:07 PM) —

3. The cit+ cultures seem to require 3 mutations.

It looks like initially only two mutations (at about 20,000 generations and about 31,500 generations) were required to give a modest advantage — the citrate-eating bacteria grew from 0.5% of the population to 19% of the population between about the 31,500th and 33,000th generations. Then the citrate-eaters nearly disappeared, and I have not seen an adequate explanation for that (the citrate eaters then started expanding again and became dominant).

Regarding some of the other comments — Sleazy PZ Myers sent some of his goons over here to harass me. My ideas about co-evolution are considered so dangerous that I was banned from discussing them on Panda’s Thumb and the blog of the Florida Citizens for Science — these ideas about co-evolution are discussed on my blog in some articles in the following group —

This group of articles may also be found by clicking on the post label “Non-ID criticisms of evolution” in the sidebar of my blog, “I’m from Missouri.” I think that this bit of self-promotion is justified by all of the derogatory comments about me in this thread. I think I am entitled to some equal time.

bunnycatch3r
June 13, 2008

This is all very exciting. It reminds of the late 1980’s when all of our world’s energy problems were solved by a discovery called “cold fusion”.

Larry Fafarman
June 13, 2008

Zachary (Blount) wrote (June 13, 2008 6:39 PM) —

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding — I will need to check with him to make certain I understand this properly). However, and unsurprisingly given that there has been only one report of a spontaneous Cit+ mutant of E. coli in the past century (Hall, B. 1982. Chromosomal mutation for citrate utilization by Escherichia coli K-12. Journal of Bacteriology, 151: 269 � 273.), none did (which wasn’t a problem – despite some misunderstanding on the internet, the intent of the experiment was never to evolve a Cit+ E. coli variant )…until, after 31,000 generations of evolution and fourteen years of the experiment, one population we call Ara-3 figured it out.

Zachary,

The following comments/questions are about the statements highlighted above.

The following two statements are contradictory —

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit

— and —

the intent of the experiment was never to evolve a Cit+ E. coli variant

I thought that the purpose of the experiment was to try to evolve a Cit+ mutant by giving the bacteria lots of citrate to eat and little glucose to eat in order to give a Cit+ mutant a big advantage.

You said,

this is my understanding — I will need to check with him to make certain I understand this properly

I am surprised that you worked with him for so long without having a clear understanding about that.

there has been only one [other?] report of a spontaneous Cit+ mutant of E. coli in the past century

Did he have an idea of what his chances of evolving a Cit+ mutant were? Did he think that by maintaining several strains of E. coli over many years, he would have a fairly good chance of evolving a C+ mutant? As it turned out, the chances were extremely poor — over a period of 20 years, the mutant evolved in only one strain out of a dozen. Lenski and his colleagues were lucky to have that one evolution.

Jesse
June 13, 2008

The bacteria possessing only the first mutation would be as likely to starve as the other bacteria that can eat only glucose.

Larry, you’re a moron.

The bacteria would also be just as likely to survive, passing on the ‘silent’ mutation to the next generation.

Go back and retake high school biology. You clearly were too busy with your finger up your nose to learn anything.

I think you need to re-read my post. I also think you need to take my suggestion to read some of the references I cited. Specifically, I think you would benefit by reading the long review of the Long Term Evolution Experiment that is reference #147 in Dr. Lenski’s publication list. You will see in it, as well as in the first paper on the experiment published in 1991 (#35), the original intent of the experiment was not evolve a citrate-utilizing variant of E. coli, but to, among other things, study the repeatability of evolution and adaptive dynamics. If you peruse the publication list on Dr. Lenski’s website, you will see that the lab has produced a large volume of research related to the original goals of the experiment and issues tangential to them.
The evolution of a citrate-utilizing variant E. coli was seen from the beginning as a possible occurrence, and one that would be pretty neat should it occur (and indeed as it has proven to be now that it has happened), but not a goal. The evolution of Cit+ in one of the twelve populations has opened new areas of inquiry in the experiment, but the experiment was never designed to bank on the evolution of that one novel trait. Much work continues to be done on the evolution of the other eleven populations in which Cit+ has not evolved. Again, I think you would benefit greatly by going to the primary, peer-reviewed literature.

Zachary

Zachary
June 13, 2008

John,

Sorry about that. I will include the spaces between paragraphs from now on. Looking up at that long post, you are right: it is hard to read. I hope you get something out of it just the same!

Trevor Murray
June 13, 2008

It has been established for some time that both selection (natural or sexual) and genetic drift are both capable of altering the proportion of genes in subsequent generations. Subsampling has also been shown to have an effect on the distribution of alleles in the resultant population, due to its inherent randomness. From what I understand this subsampling was performed daily. This event appears to be the major cause of the alteration in the distribution of neutral mutations.

I would be interested to know the estimation of the number of cells that are transferred into the new jars (sorry if it’s in the paper haven’t got to that with exams and what not atm). The low population sizes in the new jars could allow for genetic drift but this seems unlikely given that they would be well under their carrying capacity. As such population growth would be exponential until carrying capacity is reached. During exponential growth we expect no difference in the mean growth rate between carriers of genetically neutral mutations; the only differences would be in those that have beneficial or disadvantageous mutations. I guess if there is significant time between taking the sample and placing it in the new jar (multiple generations) then drift could occur at this stage.

Again I’d like to thank the authors for their awesome and thought provoking experiment.

Zachary
June 13, 2008

Trevor,

The populations reach approximately 300 to 500 million cells at their maximum (save for Ara-3, the one in which the Cit+ variant occurred, which now reaches approximately ten times that number) each day. The populations are grown in 50 mL flasks. Each day at the time of transfer, we dispense 9.9 mL of fresh medium into thirteen sterile flasks. One of these is the blank, and no bacteria are added to it. To the each of the other twelve are then transferred 0.1 mL (100 microliters) of the populations from the previous day’s cultures. We transfer the populations immediately after removing them from the incubator, and the newly inoculated cultures then go right back into the incubator. As you likely already figured out, around 3 to 5 million cells are transferred each day per population (again, save for Ara-3, for which the 1% transferred contains ten times as many cells).

While drift can still be an issue, and one cannot ignore the possibility of the loss of even weakly beneficial mutations during transfer (especially of a new mutation that had occurred during the last generation of the previous day), it is not as much an issue as it would be if the population sizes were not as large as they are. Does that answer your question sufficiently? As I recall, Dr. Lenski discusses the issue of drift in the experiment in publication #147 of the complete list on his website (which is available as a pdf). When you get finished with your exams, you might want to take a look. In the meantime, thank you for the compliment, and good luck with the exams. At this point my only remaining exam is going to be my thesis defense, but I have felt your pain many, many times in the past.

Thank you,
Zachary

Ian Fisk
June 13, 2008

When I first heard about this experiment I thought that is was totally awesome.

Now I realize that it must really blow the minds of creationists. Their choices are either
A citrate-utilizing variant E. coli evolved though mutation and natural selection.
or
A citrate-utilizing variant E. coli was created by the actions of God. The ability to replay the experiment means that scientists can control the actions of God!

Trevor Murray
June 13, 2008

Zachary,

Thanks for that. Yes that answers pretty much everything. As you say those population sizes are still extremely large at all stages so loss is unlikely for all but the rarest (extremely low proportion of populaiton) of mutations. at bottleneck of 3-5 million cells isn’t really a bottleneck at all. I’ll definatly be reading that paper as soon as I get back from my behavioural ecology exam this afternoon. It doesn’t look like your going to have any problems with that thesis defense. You’ll probly spend most of you time anwering the questions the examiners are interested in.

Thanks again
Trev

Larry Fafarman
June 14, 2008

Zachary said in comment # 122 (June 13, 2008 10:28 PM) —

Larry,

I think you need to re-read my post.

Thanks for answering my comment.

I read your post right the first time — there is an inconsistency in your statements (see my comment #119).

I also think you need to take my suggestion to read some of the references I cited.

There is an awful lot to read there and I might not find the answers to my questions. And in any case, I would still be confused by your comment #115.

The evolution of a citrate-utilizing variant E. coli was seen from the beginning as a possible occurrence . .

But you said in comment #115 that you were unsure of that:

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding — I will need to check with him to make certain I understand this properly).

I am not saying that trying to evolve citrate-eating E. coli was the sole purpose of the experiment, but the experiment appears as if it was set up to favor such evolution — the bacteria were grown in a citrate-rich medium and were given an insufficient supply of glucose. The original post says that the supply of glucose for daily cultures started in the morning would be “gobbled up by the afternoon”:

Lenski started off with a single microbe. It divided a few times into identical clones, from which Lenski started 12 colonies. He kept each of these 12 lines in its own flask. Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose.

If the purpose of the insufficiency of the glucose supply was not to promote evolution of citrate-eating E. coli, then may I ask what the purpose was?

Zachary said in comment #125 (June 13, 2008 10:47 PM) —

Each day at the time of transfer, we dispense 9.9 mL of fresh medium into thirteen sterile flasks. One of these is the blank, and no bacteria are added to it. To the each of the other twelve are then transferred 0.1 mL (100 microliters) of the populations from the previous day’s cultures. . . .

one cannot ignore the possibility of the loss of even weakly beneficial mutations during transfer (especially of a new mutation that had occurred during the last generation of the previous day)

Considering that there are just a few generations per population and that only one percent of an old population is transferred to start a new population, I suspect that a lot of mutations are lost because of failure to be transferred (there were probably very few generations of glucose-eating-only bacteria in each population because glucose-starvation probably inhibited reproduction). Maybe that is why the mutations of the citrate-eaters took so long to appear in one of the strains and why those mutations did not appear at all in the other 11 strains.

Zachary
June 14, 2008

Larry,

Again, I suggest you go and read reference #147 as well as the citrate paper itself. They will answer most, if not all of your questions.

Zahcary

Larry Fafarman
June 14, 2008

Jesse driveled,

The bacteria possessing only the first mutation would be as likely to starve as the other bacteria that can eat only glucose.

Larry, you’re a moron.

The bacteria would also be just as likely to survive, passing on the ‘silent’ mutation to the next generation.

You’re the moron. Just as likely to starve, just as likely to survive, what’s the difference? The point is that there is no natural selection here driving evolution.

All you Darwinists can do is insult people — that’s why you have no credibility.

slang
June 14, 2008

Good ole larry.. knows the law better than a judge, knows every single area of science better than scientists that spent their careers in it, builds strawmen for a hobby and he has a dictionary. Beware!

Trevor Murray
June 14, 2008

Just finished reading the paper. Fantastic. Great work Zachary (and co authors) it was both easy to follow, interesting and very infomative. You guys did so many experiments to cover different angles and differentiate between hypotheses. I really can’t wait to see what the future experiments are going to show.

Trev

andy
June 14, 2008

Larry casts aspersions on this fine experiment at peril of highlighting the experiment’s confirmation of original prediction of Darwin: the response of a population to changes in environment.

Rob
June 14, 2008

this research makes me feel warm and fuzzy inside. i love good science.

larry, you are a tool. I laugh myself to sleep every night knowing that you are unable to grasp basic science

Larry Fafarman
June 14, 2008

Zachary said,

Again, I suggest you go and read reference #147 as well as the citrate paper itself. They will answer most, if not all of your questions.

I still have this question that I don’t think reading the literature will answer. You said,

The evolution of a citrate-utilizing variant E. coli was seen from the beginning as a possible occurrence, and one that would be pretty neat should it occur (and indeed as it has proven to be now that it has happened), but not a goal. (emphasis added)

But it appears that evolution of a citrate-utilizing variant E. coli was a goal because it appears that the experiment was set up to promote such evolution — lots of citrate and insufficient glucose.

website design
June 14, 2008

Gradualism has been on its way out for a while now.

website design
June 14, 2008

Gradualism has been on its way out for a while now.

web design company
June 14, 2008

Gradualism has been on its way out for a while now.

website design
June 14, 2008

Gradualism has been on its way out for a while now.

Larry Fafarman
June 14, 2008

Lousy trolls Slang, Andy, and Robb:

As I said, you Darwinists have no credibility because all you can do is insult people.

I have a right to comment or ask questions in any field — science, law, etc.. And my comments and questions here are very basic.

I propose that we don’t teach Darwinism to students who don’t plan on going into biology. After all, students who don’t become biologists won’t need Darwinism in their jobs and won’t be qualified to discuss Darwinism. And let’s not bother teaching students about the Constitution unless they plan to become lawyers. Etc., etc..

Website design:

What does this have to do with gradualism?

noncarborundum
June 14, 2008

Larry –

Why does it matter whether the evolution of citrate utilization was a goal or not? Are the bacteria going to behave any differently than if the goal were, say, to see how fast the bacteria would die off in a medium they couldn’t exploit?

tyrone slothrop
June 14, 2008

I don’t think I have ever seen a better example of the level of scholarship of those who challenge legitimate research than the following statement by Larry:

“There is an awful lot to read there and I might not find the answers to my questions.”

There is an awful lot to read. That, after all, is what scholarship is about. And the second part of the statement reveals the lack of intellectual curiosity. Larry sounds like an undergrad.

Larry Fafarman
June 14, 2008

noncarborundum said,

Larry –

Why does it matter whether the evolution of citrate utilization was a goal or not?

I am just curious — is there anything wrong with that?

There is an inconsistency here. Zachary said that evolving citrate-eating E. coli bacteria was not a goal of the experiment but the experiment appears to have been set up to promote such evolution. No other explanation for the setup of the experiment has been given.

I can certainly believe that evolving citrate-eating E. coli bacteria was not the sole purpose of the experiment because otherwise I think the experiment would have been abandoned because no citrate-eating bacteria appeared for many, many years (the first appeared at around 14 years).

noncarborundum
June 14, 2008

I am just curious — is there anything wrong with that?

Not in the abstract, but you appear to be casting about for holes to poke, so I question the sincerity of your curiosity. If I’m wrong about this I beg your forgiveness.

I notice that you didn’t answer the question I posed to you: what difference would it make if the evolution of citrate utilization had been a goal?

Zachary
June 14, 2008

Hi everyone,

My responses here are likely going to taper off in lieu of putting together a post for Carl to put on the website. Hopefully it will answer most of the questions out there that those with a good faith interest in the research. In the meantime, I would like to again invite everyone to read the citrate paper itself. For those with further interests concerning the long term evolution experiment, its goal and objectives, design, logistics, and findings, I would suggest again that you go to Dr. Lenski’s webpage at https://www.msu.edu/~lenski/ where you will find a great many of the papers published on the LTEE in free, pdf format. The best place to start is with publication #147 on the complete list of publications. Another good paper to read to start out is publication #145, which is a review of the use of microbes as experimental model systems with which to study evolution in action. You will find in both good, lucid discussions of the roles of natural selection and drift in these experiments (Trevor, if you are still out there, there is a paragraph in #145 on page 459 that deals specifically with the effects of drift). You should branch out from those papers to the ones they cite on specific experimental issues and questions as your interests and curiosity compel you.

As I have noted earlier, whenever one has significant, substantive interest in any research, it behooves one to go to the primary, peer-reviewed literature on that research. It constitutes the official and most detailed reports and descriptions, and many, if not most issues may be resolved by recourse to them. While popular accounts and forums such as this are good places to start, they are no substitute for the original papers themselves. It is said that when asked by King Ptolemy for an easier way to learn mathematics, Euclid replied,”There is no royal road to geometry.” That is as true of evolutionary biology as it is of any science or difficult field of intellectual endeavor. It is true also that an uninformed understanding is not understanding at all.

Good luck, thank you, and happy reading (it’s difficult, yes, but quite rewarding). I hope to have something for Carl in the next few days.

Zachary

Larry Fafarman
June 14, 2008

noncarborundum said,

Not in the abstract, but you appear to be casting about for holes to poke, so I question the sincerity of your curiosity.

This is not just “casting about for holes to poke” — my question is basic. Because the experiment was conducted with lots of citrate and insufficient glucose, I originally thought that a goal of the experiment was to evolve a Cit+ mutant. Now Zachary is saying that was not a goal. My question is a fair one. By asking me to just read the literature, Zachary is trying to send me off on a wild goose chase in order to avoid answering a simple, basic question.

I notice that you didn’t answer the question I posed to you: what difference would it make if the evolution of citrate utilization had been a goal?

What is so wrong about wanting to understand the purpose(s) of an experiment?

And it is not just a matter of whether or not evolving citrate-eating E. coli bacteria was a goal. If there was some other reason for conducting the experiment in that manner — lots of citrate and insufficient glucose — I would like to know what that reason was.

Trevor Murray
June 14, 2008

Larry

Zackary stated in 115# that the excess of citrate was: a) a contingency based on decades of previous research in growing e. coli, b) primarily to allow e. coli to absorb iron via a chemical pathway, c) at higher consentration than otherwise necessary to prevent precipitation of magnesium sulfate. These 3 points clearly show a function for the high levels of citrate other than “to produce citrate eating bacteria”. There is a similar occrence in evolution called exaptation. Somthing develops for one purpose (to produce an environment suitable to e. coli growth where the exact properties are understood) and is coopted by evolution for a different function (allowing the development of cit+ mutants). It is clear that the goal of the experiment was not to produce Cit+ mutants, though this was a very interesting phenominon that provides experimental evidence for biological theory. This can be shown from looking at the original proposals as well as the wealth of papers that have already been written.

Trev

Trevor Murray
June 14, 2008

Oh man I only just got what Zachary meant by hijacking. That makes sense as to the fixation of the original (gen. 20,000) mutation. The other thing I was thinking is it could be a beneficial mutation that was only beneficial in light of the other mutations present in that line. For example say it was a gene duplication of a transporter channel protein for glucose. In this case it would be advantageous if more channels an improvement for glucose digestion and so it would slowly grow to fixation. If however there was another mutation present in other lines say an upregulation of the transporter channel that results in increased production of the channel protein, then the increase due to gene duplication wouldn’t be an advantage. They would already have enough of the channels due to the additional production due to upregulation. I guess this would be another example of contingency.

As Zachary states if the first mutation is a channel protein gene duplication, then the following mutations must alter it to make it amiable to citrate transport. This seems (to me) to be consistent with the growth rate comparison where in the same population Cit- growth fast at first then plateaus and Cit+ growth slowly on glucose then switches to citrate and keeps on growing (I may have the switching thing wrong though). If it was the conversion of second glucose channel it would decrease their growth in the glucose phase, but once it switched to citrate they would gain the advantage.

Well this is just conjecture and I

Alan Kellogg
June 15, 2008

Shorter Fafarman

This is hard!

Larry Fafarman
June 15, 2008

Trevor Murray said (#147)

Larry

Zackary stated in 115# that the excess of citrate was:

Have you been reading what I have been writing? I said that I am not just concerned about the citrate — I am also concerned about the reason for giving the bacteria an insufficient supply of glucose. I said that I previously assumed that the bacteria were given insufficient glucose in order to promote evolution of C+ mutants by giving them a big advantage over the bacteria that could eat only glucose. Zachary’s responses have been very inconsistent about whether evolving C+ mutants was a goal of the experiment —

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding – I will need to check with him to make certain I understand this properly). (comment #115)

the intent of the experiment was never to evolve a Cit+ E. coli variant (comment #115)

The evolution of a citrate-utilizing variant E. coli was seen from the beginning as a possible occurrence, and one that would be pretty neat should it occur (and indeed as it has proven to be now that it has happened), but not a goal. (comment #122)

It is clear that the goal of the experiment was not to produce Cit+ mutants

The issue here is not just whether that was the only goal, but also whether that was one of the goals if there was more than one.

If promoting evolution of C+ mutants was not the reason for giving the bacteria insufficient glucose, then I would like to know what the reason was.

If one of the paper’s co-authors won’t give direct answers to very simple questions, then the paper has no credibility. That’s all there is to it.

Trevor Murray
June 15, 2008

Larry

You are right there must have been a reason for having insufficient glucose, unfortunately its not to promote Cit+ evolution. In fact it

Apostasius
June 15, 2008

One possible source of confusion that Larry may have is the lack of differentiation between the Lenski Long Term experiment and the work that Zachary has done.

My understanding is that the long-term evolution experiment(LTEE) set up 20 years ago did not have as its purpose to evolve a cit+ mutant. I assume Dr. Lenski was aware of the possibility (however remote) that E. coli could evolve to use citrate as a carbon source, but I am sure he also had several other ideas about what might or might not happen. The deck was not stacked.

When the Ara-3 population was examined (due to what appeared to be contamination), the investigation revealed an interesting possibility/question. Like all good research, further experiments were done leading to the exploration of a cit+ variant. Zachary’s work is a subset of the LTEE–not the LTEE itself. His work did involve re-evolving (replaying the tape) the Ara-3 line (grown separately from the LTEE using the frozen fossil record). Perhaps this is the source of confusion that Larry has.

Trevor Murray
June 15, 2008

A good point.

Kieran Lerch
June 15, 2008

“By asking me to just read the literature, Zachary is trying to send me off on a wild goose chase in order to avoid answering a simple, basic question.”

Larry, you seem to be coming into this with the idea that Zachary has the intent to mislead you. Why is that? And why is it that you think the literature itself will not answer your question about what the goals of the experiment were? You seem to have a lot of concern about these issues; well, reading is what people in the sciences spend a lot of time doing. Reading is essential, and even without reading this specific paper, an education in the subject that seems to interest you so much might just answer your questions by providing information such as Trevor’s in #151.

Larry Fafarman
June 15, 2008

Trevor and Apostasius,

I wanted Zachary to answer the questions. His answers are mutually contradictory and he referred me to the literature without giving links and/or page numbers where my questions are discussed.

Trevor said,

Larry

You are right there must have been a reason for having insufficient glucose, unfortunately its not to promote Cit+ evolution.

How do you know that that was not at least one of the reasons? It is the most obvious reason. This article, for example, appears to assume that that was at least one of the reasons:

In 1988, Richard Lenski, Michigan State University, East Lansing, founded 12 cultures of E. coli and grew them in a laboratory, generation after generation, for twenty years (he deserves some marks for persistence!). The culture medium had a little glucose but lots more citrate, so once the microbes consumed the glucose, they would continue to grow only if they could evolve some way of using citrate. Lenski expected to see evolution in action.

Trevor said,

In order for natural selection to occur there must be differential reproduction.

Natural selection may also involve differential death rates (which are tied to differential reproduction if individuals do not survive long enough to reproduce)

Where there is lots of citrate and an insufficient supply of glucose, the most biggest and most obvious cause of differential reproduction would be development of the ability to eat citrate!

Rate of reproduction allows e. coli to produce more offspring faster than their competitors

Yes — the evolution of faster-breeding bacteria was observed.

In order to ensure that differential survival is a major factor in the evolution of the e. coli the authors has to ensure that the carrying capacity of the environment can be reached.

Do bacteria start to die of starvation within a few hours? I think that bacteria in general can live indefinitely or a long time without food. I think that the primary effect of lack of food would be inhibition of reproduction.

During the first phase (when glucose is plentiful) the e. coli reproduce exponentially. It is only after they reach the carrying capacity that competition occurs in earnest and a greater selection pressure can be imposed. In this secondary stage there are many ways that strains can gain an advantage: glucose digestion efficiency, digestion of dead e. coli, production of chemicals that decrease survival of competitors; to name just a few. Yes cit+ is one of these potential outcomes but it is only one of many.

Higher efficiency in digesting glucose could result in higher reproductive rates before the glucose supply runs out but does no good after the glucose supply runs out. And the most obvious alternative food supply is citrate. Cannibalization of other bacteria (which I think has been observed) is a much less obvious alternative source of food.

There is a big difference between a potential outcome and a goal. A goal is a defined end point to an experiment that the experiment hinges answering. A potential outcome is not necessary for the experiment, they can be interesting and useful but the experiment does fine without them.

That is doublespeak. If evolution of C+ mutants was foreseen as a possible and desirable outcome (it obviously is a desirable outcome), then by definition it was a goal. It would be a goal even if the design of the experiment were not wholly or partly based on trying to achieve that goal.

I will ignore your final statement.

That figures.

Hardline Darwinist roaders are claiming that this paper is absolute proof that Darwinism is true. This paper is being used to attack the ideas of Michael Behe. I want the whole world to know that this paper lacks credibility because a co-author of the paper is stonewalling some very simple questions about it.

I realy hope that answers your questions

No, it does not. And even if it did, I would still be unsatisfied because I want Zachary to give straight and consistent answers to the questions.

Apostasius said,

My understanding is that the long-term evolution experiment(LTEE) set up 20 years ago did not have as its purpose to evolve a cit+ mutant.

How do you know? Are you sure?

And I said that I am not just asking if that was the sole purpose — I am also asking if that was one of the purposes if there was more than one. Don’t you people read what I write?

rrt
June 15, 2008

Precisely, Kieran. But Larry doesn’t actually want to educate himself. He wants to childishly stamp his foot and demand to be spoon-fed pre-chewed answers (but only the kinds he wants to hear!)

I appreciate the good-faith efforts of some here to educate Larry, but I guarantee you he doesn’t. Larry can’t be bothered to approach science…well…scientifically, such as with the standard practice of reading the research upon which one wishes to opine. After all, there’s a lot to read there, and it might not have the answers he wants to hear.

Larry’s on a fishing expedition here for excuses to declare fraud or incompetence. And to Larry, an experiment that sets up an environment favorable for evolution of certain traits counts as cheating.

Larry Fafarman
June 15, 2008

Kieran Lerch said,

Larry, you seem to be coming into this with the idea that Zachary has the intent to mislead you.

He is not trying to “mislead” me — he is not trying to lead me at all! Either he won’t answer my questions at all or he gives inconsistent answers — see my comment #150.

And why is it that you think the literature itself will not answer your question about what the goals of the experiment were?

I should be given links and page numbers (if the articles are long) to the places where my questions are answered. Instead I am just sent off on a wild goose chase.

You lousy dunghill, what do you mean that I don’t actually want to educate myself. I have spent many hours reading reviews and comments about this paper. And I don’t have to educate myself before asking a question.

And to Larry, an experiment that sets up an environment favorable for evolution of certain traits counts as cheating.

Dummox, one of the questions I asked was whether the reason or one of the reasons for the insufficiency of the glucose supply was to set up an environment favorable for evolution of a citrate-eating trait.

I have some questions that I want to ask about the results of the experiment, but I am now wondering if I should bother asking them.

Kieran Lerch
June 15, 2008

Wait, you’ve spent many hours reading reviews and comments about this paper but you haven’t read the paper itself? If the time and energy of typing questions and responses and reading the comments about the paper isn’t a barrier to doing so, why shouldn’t you have just read the paper to begin with?

Larry Fafarman
June 15, 2008

Kieran Lerch said,

Wait, you’ve spent many hours reading reviews and comments about this paper but you haven’t read the paper itself?

The paper is long, detailed and complicated. Until very recently, it was pay-per-view. I read the abstract of the paper. Most people who have commented on the paper have not read it — you people are just singling me out for not having read the paper. And I don’t need to read the paper before asking questions about it.

Owlmirror
June 15, 2008

Reference #147 and #145 on Lenski’s publications page, with direct download links to PDFs of the publications. Because browsing the web is so hard.

True, but you might need to read it, and especially the peripheral publications explaining the larger experiment of which this is but a part, before asking useful questions, Larry.

And I’m sorry, Larry. A dummox like me can’t figure out how that addresses my point. You asked what the reason for limited glucose and lots of citrate was…why? Seems awfully important to you whether it was a primary, initial goal to evolve citrate-eating or not.

Why?

rrt
June 15, 2008

No no no, Owlmirror. He wants chapter and verse. Preferably posted by the primary authors themselves.

tyrone slothrop
June 15, 2008

This reads like the worst of my undergrads (the very worst).

“I should be given links and page numbers (if the articles are long) to the places where my questions are answered.”

Notice what is important here. Not the research, not the scholarship, but rather the “I”. The “I” having not done actual research and further not wanting to do the actual reading of the research, “should be given”–spoon fed I guess–the answers. There is no desire here for scholarship. Just ego.

When I was in grad school, if I had said that to my advisor, I would not have earned my phd.

Larry Fafarman
June 15, 2008

True, but you might need to read it, and especially the peripheral publications explaining the larger experiment of which this is but a part, before asking useful questions, Larry.

My questions are useful, dunghill.

You asked what the reason for limited glucose and lots of citrate was…why?

Let’s suppose that I don’t really “need” an answer to that question. King Lear said in Shakespeare’s play,

O reason not the need!
Our basest beggars
Are in the poorest thing superfluous.
Allow not nature more than nature needs,
Man’s life is as cheap as beast’s. Thou art a lady:
If only to go warm were gorgeous,
Why, nature needs not what thou gorgeous wear’st,
Which scarcely keeps thee warm. But, for true need–
You heavens, give me that patience, patience I need.

Anyway, Zachary gave reasons for the citrate but I am wondering if trying to evolve C+ mutants was another reason for the citrate. Zachary gave no reason for the limited glucose.

No no no, Owlmirror. He wants chapter and verse.

In legal citations, the document name, location, and page number(s) are given, dunghill.

Reference #147 and #145 on Lenski’s publications page, with direct download links to PDFs of the publications.

I have a slow dial-up connection and PDF’s sometimes take several minutes to download and sometimes don’t download at all. That slows me down and often I can’t get stuff at all.

Notice what is important here. Not the research, not the scholarship, but rather the “I”. The “I” having not done actual research and further not wanting to do the actual reading of the research, “should be given”–spoon fed I guess–the answers. There is no desire here for scholarship. Just ego.

When I was in grad school, if I had said that to my advisor, I would not have earned my phd.

Of course I said “I,” idiot, I was the one who asked the questions! And if I had said “we” instead of “I,” some jerk would have told that tired old Lone Ranger joke, “what do you mean, ‘we,’ paleface?” I just can’t win.

I am not working on a Ph.D. and this subject is not my only interest.

You idiot, what if the citations in your dissertation or other papers had said, “go find it yourself”?

Also, my question about whether evolving C+ mutants was a goal (or something that was hoped for or wished for or whatever) leads to another question: If it was a goal, particularly an important goal, then why were the populations restarted so frequently, i.e., every day? Starving the glucose-only bacteria for a longer time would have increased the advantage of C+ mutants. Also, restarting the populations daily was demanding (what about weekends and holidays?) and increased the labor requirement, which added up after 20 years.

If there was no particular reason for doing something a certain way in the experiment, then why can’t I just be told that there was no particular reason.

I wonder — do you idiots give this kind of crap to peer-reviewers of your papers?

tyrone slothrop
June 15, 2008

No Larry, you are not working on your phd. That is quite obvious. And your responses shows why you are not. You simply lack the dedication, the hard work of actual scholarship. The dissertation comes after a great deal of work, of scholarship and research. That seems lost on you.

Sometimes, peer-reviewers will tell you to go look at an article. They will not tell you what page to look on. They assume that you will read the article and make the connections. Zachary gave you too much credit. I do not.

Larry Fafarman
June 15, 2008

tyrone slothrop barfed,

No Larry, you are not working on your phd.

Right. So why should I be expected to read all the literature in this field as though I were working on a Ph.D in this field? I have other interests. Even so, I have devoted a lot of time to reading the reviews and comments about this paper.

Anyway, as I said, most of those who have commented on this paper did not read it and did not read a lot of the other scientific papers on the subject, so I am being singled out for criticism.

Sometimes, peer-reviewers will tell you to go look at an article. They will not tell you what page to look on.

Sometimes that’s appropriate — it was not appropriate in my case because my questions were simple and very specific.

Zachary gave you too much credit.

Zachary did not give me any credit — he either did not give consistent answers to my questions or he did not give any answers at all.

You are lazy. You wanted things handed to you. You are not willing to do the scholarship needed to understand the research. Why should anyone take you seriously? Zachary gave you too much credit. I do not. I do not take you seriously. You complain like a very spoiled undergrad. And you deserve to be treated accordingly.

Forget grad work. If I’d tried to behave like you do in high school, I’d have failed the class. If you have so little interest in the subject that you can’t be bothered to actually read up on it, then stop trying to pretend you’re profound.

Rob
June 16, 2008

Larry,

why don’t you just get over it and read the paper? are there any conclusions in there that would enable you to overcome your ID background and accept evolution? if not, than your really just wasting everyone’s time, coming in here with a preconcieved notion of what is going on and debating fine points that are not issues for anyone else. It seems that you want Zachary to come in and tell you exactly what the cit was doing in the flask and the limited glucose, even though several other people have explained for you. I would theorise that Zachary won’t, because that will give you and your preconcieved conclusions legitimacy.
read the paper, come to a better understanding of the conclusions, and live with it.

Stephen Couchman
June 16, 2008

Zachary, you’re a fricken’ rock star.

Eat it, Behe. Tell us how it tastes.

Stephen Couchman
June 16, 2008

Larry @ 164

“Also, my question about whether evolving C+ mutants was a goal (or something that was hoped for or wished for or whatever) leads to another question: If it was a goal, particularly an important goal, then why were the populations restarted so frequently, i.e., every day? Starving the glucose-only bacteria for a longer time would have increased the advantage of C+ mutants.”

I may be misunderstanding you, but you seem to be under the impression that Lenski et al threw out each generation of e coli after one day of observation. The following excerpt is from the second paragraph of the article you’re commenting on (emphasis mine):

“Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. And on and on and on, for 20 years and running.”

Nothing was “restarted.” Each new day’s sample was “legacy bacteria” descended from the previous day’s batch. The reintroduction of a starter colony to a supply of glucose didn’t reboot the scarcity experiment because the initial amount of glucose was scarce compared to population size already. The daily re-sampling was for the benefit of the researchers tracking bacterial generational data over human-scale time. Additionally, they archived generations and revisited them to found new descendant populations, which is how the Cit+ adaptation was recreated.

I don’t have the history reading your comments that some of the regulars and other guests on this blog seem to have, but it spoke volumes when you spouted:

“Hardline Darwinist roaders are claiming that this paper is absolute proof that Darwinism is true. This paper is being used to attack the ideas of Michael Behe. I want the whole world to know that this paper lacks credibility because a co-author of the paper is stonewalling some very simple questions about it.”

This after post upon post about how you just want your questions answered to satisfy your intellectual curiosity.

Neither of us is a qualified scientist. You write coherently, though not cogently, so I’m guessing your reading comprehension is at least as good as mine. Is it your argumentative tone and rush to insert your agenda into the dialog that makes these points clear to me and obscure to you? Let’s run an experiment: I’ll read science blogs without a bias in favor of shoddy, populist nonsense-theories (look, I’m your control group!), and you keep going the way you’re going. In a year, we’ll see who can wring more understanding out of a scientific paper . . . or a lay-accessible article about one.

John Morales
June 16, 2008

Zachary, I applaud your efforts, but I think I’ve gained some insight and reassurance about the value of your work rather than advanced biological knowledge

—

Zachary did not give me any credit — he either did not give consistent answers to my questions or he did not give any answers at all.

On the contrary, Larry; Zachary generously pointed you to reference #147 (just over 2Mb*) which is a review of the experiment and explicitly sets out its basis and goals.

*You’ve probably downloaded more than that in refreshing this page and commenting…

When I think of environmental stressors that tend to induce mutations, I think of ionizing radiation and irritating chemicals. I don’t think of starvation in that way.

And a lot of you Darwinists just can’t discuss anything without insulting people.

Stephen Couchman said (#172) —

I may be misunderstanding you, but you seem to be under the impression that Lenski et al threw out each generation of e coli after one day of observation.

No, I was never under that impression.

The time when the citrate-eating bacteria have an advantage over the bacteria that can eat only glucose is of course the time after the glucose has been exhausted. The glucose is exhausted in a few hours (“Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon”). Extending the lives of the populations (now one day) would increase the ratio of (1) the time when there is no glucose to (2) the time when there is glucose, thus increasing the citrate-eating bacteria’s overall advantage over the bacteria that can eat only glucose. That was my point.

“The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose.”

I am concerned about mutations being lost because (1) only one-percent of old populations were transferred to start new populations and (2) there were few generations per population. Even Zachary expressed concern about this — he said,

. . . one cannot ignore the possibility of the loss of even weakly beneficial mutations during transfer (especially of a new mutation that had occurred during the last generation of the previous day) . . .

I said, “This paper is being used to attack the ideas of Michael Behe.” You said (#171),

This after post upon post about how you just want your questions answered to satisfy your intellectual curiosity.

Is there something wrong with having intellectual curiosity?

You write coherently

Thanks for the compliment.

Is it your argumentative tone and rush to insert your agenda into the dialog that makes these points clear to me and obscure to you?

Trying to get straight and consistent answers to simple questions is being argumentative?

Rob said (#170) —

Larry,

why don’t you just get over it and read the paper?

Why can’t Zachary just answer my simple questions (others have tried to answer but they can’t always speak for Zachary and the answers have mostly not been satisfactory)? Why do I have to wade through a lot of stuff unrelated to my questions? And I might not find answers to some questions anyway.

if not, than your really just wasting everyone’s time, coming in here with a preconcieved notion of what is going on and debating fine points

I did not come in here with a “preconceived” notion and my points are basic, not fine.

tyrone slothrop
June 16, 2008

“Why do I have to wade through a lot of stuff unrelated to my questions?”

Perhaps, by actually reading the research, you might learn something. But learning something is not what this is about for you. You complain like a spoiled undergrad.

You have not exhibited any intellectual curiousity. That is one of your problems. You seem too intellectually lazy for that. And you should be treated accordingly.

Rob
June 16, 2008

Larry said
When I think of environmental stressors that tend to induce mutations, I think of ionizing radiation and irritating chemicals. I don’t think of starvation in that way.

time you thought of it in that way

Cynthia Wood
June 16, 2008

Larry – I say “Sheesh”, you say that Cynthia Wood “drivels” and I’m the insulting one?

Any environmental stressor is fair game. Irradiation is a stressor that also could increase the mutation rate, hence not as satisfactory. In fact, I would imagine that if such a thing were used and a similarly striking mutation found then you, or people like you, would be complaining that the evolutionary changes had only occurred because of the irradiation and the results were invalid under more normal conditions. Lack of food, otoh, is one of the single most common environmental stressors you can find in virtually any wild population of anything.

As for the high school comment, it’s nothing but straight up truth. I had to write research papers that involved reading original sources, no predigested summaries, no getting other people to come up with the answers for me, actual understanding of the material required to be shown. If I had gone to my teachers with the kinds of demands you’ve been making here (or even my parents had they told my teachers about it), I would have failed the paper and probably been booted back a track. And these were people with a relationship with me and an obligation to my learning future.

FO
June 16, 2008

I propose that we don’t teach Darwinism to students who don’t plan on going into biology. After all, students who don’t become biologists won’t need Darwinism in their jobs and won’t be qualified to discuss Darwinism. And let’s not bother teaching students about the Constitution unless they plan to become lawyers. Etc., etc..

I propose that we don’t teach basic Arithmetic to students who don’t plan on going into mathematics. After all, students who don’t become mathematicians won’t need Arithmetic in their jobs and won’t be qualified to discuss Arithmetic.

o_O

I wanted to believe Fafarman’s post was sarcasm, but apparently it’s not.

Is this guy for real?

Larry Fafarman
June 16, 2008

Try as hard as you might, trolls, you can’t justify a researcher’s refusal to answer some simple, basic questions about his research.

Perhaps, by actually reading the research, you might learn something.

As I said, most people who have commented about the study have not read the paper. I am being singled out for criticism.

Here it is actually more important to read the reviews and comments about the study than it is to read the paper itself, because those reviews and comments are where most people are getting all of their knowledge about the study. There have been several reviews and hundreds of comments about the study. And as I said, I don’t plan on making a career of studying this subject.

Larry saidWhen I think of environmental stressors that tend to induce mutations, I think of ionizing radiation and irritating chemicals. I don’t think of starvation in that way.
time you thought of it in that way

I have never heard that starvation can induce mutations. Anyway, I doubt that a few hours of starvation is a particularly high stress for these bacteria. And if this was a purpose for starving the bacteria, then Zachary should say so. And he never gave an answer to the question of whether the glucose starvation was intended to promote evolution of Cit+ mutants by giving them an advantage over bacteria that could only eat glucose.

Larry – I say “Sheesh”, you say that Cynthia Wood “drivels” and I’m the insulting one?

“Sheeesh” was not a reason why I called your comment insulting.

Lack of food, otoh, is one of the single most common environmental stressors you can find in virtually any wild population of anything.

I was talking about environmental stressors that tend to induce mutations. I got no answer to my question about whether glucose starvation was an environmental stress that was intended to give an advantage to Cit+ mutants.

If I had gone to my teachers with the kinds of demands you’ve been making here (or even my parents had they told my teachers about it), I would have failed the paper

There’s no comparison — I am just asking a researcher some questions about his research. I am asking questions that only he or one of his fellow researchers can answer.

Larry Fafarman
June 16, 2008

FO said,

I propose that we don’t teach basic Arithmetic to students who don’t plan on going into mathematics. After all, students who don’t become mathematicians won’t need Arithmetic in their jobs and won’t be qualified to discuss Arithmetic.

I wanted to believe Fafarman’s post was sarcasm, but apparently it’s not.

Is this guy for real?

Yes, I’m for real. Are you?

People who are not biologists or lawyers can get by quite well without knowing anything about Darwinism or the Constitution (even many biologists do not need to know anything about Darwinism). In fact, I heard of a survey where people were asked to name some freedoms or rights protected by the Bill of Rights, and a large percentage of people could not name a single one — if they had named just one, say, freedom of speech, they would have gotten credit for successfully answering the question. However, people need to know something about arithmetic just to handle money.

Cynthia Wood
June 16, 2008

Larry – how are people supposed to find out that they want to be biologists, chemists, mathematicians, lawyers, or pretty much anything if they’re never exposed to these subjects in even elementary form? Whether they remember it well later is somewhat of a separate issue – though I wish greatly that some people did remember their grade-schooling better.

I didn’t take Calculus in high school because of my burning need for calculus in my later life, but because several fields that would have required calculus were still possibilities and I found it interesting. You never know just what subject is going to fire a child’s passion.

Plus what a gray and impoverished world we would live in if education were limited to only the practical.

Hoovooloo
June 16, 2008

Mr. Fafarman,
Now, I will admit I have not read the paper. I have, however, learned a fair bit about biology (I’m still in college, so I cannot claim to have worked in the field), and hope to help in this discussion.

First of all, you seem to question if seeing Cit+ was a goal of this experiment, and if so, it would invalidate the experiment as evidence against Behe. From what I understand, Behe claims that the likelihood of complex traits evolving is so low, it indicates the presence of a creator to guide the evolution. Now, this is different from claiming that the environment was designed by a creator in a manner that is unsuited to the organism. Behe’s point seems to be that, given the probability of a single mutation occurring, there is almost no chance that a complex trait could evolve. Thus, a creator must be directing evolution at an almost molecular level, to influence these probabilities to a degree beyond natural influences.

With this experiment, they set up an environment to which the organism is poorly suited. Again, this does not seem to be what Behe means when he claims the presence of a creator, so this feature alone does not invalidate the experiment. This feature is also necessary, as if there were plentiful glucose, if the organism was well suited to the environment, there would be little pressure for it to evolve, and the experiment would take far longer than a human could observe. As others have mentioned, changes in the environment can produce these situations in nature, so the experiment is still valid. As for what was used to induce the mutations, it would seem the experimenters did nothing. They relied on ionizing radiation, transcription errors, and other natural causes to produce said mutations. Since the experimenters did nothing to directly manipulate the evolution of the bacteria, and the environment in the experiment could have occurred naturally, the fact that a complex new trait evolved would seem to refute Behe, even if the experimenters had hoped to see this trait evolve.

On the note of reading papers, you seem to want a paper that answers, on a single page, these questions that you call basic. However, many papers will not do this, instead spreading the explanation out over many pages, explaining a bit more as they describe each piece of evidence. Thus, it may be necessary to read the whole paper to fully understand the answer. The reason you are being “singled out” is that, when you were linked to papers that people claim would answer your questions, you refuse to read them, either on the ground that they are too long or they would take “minutes” to download. That you continue to demand answers, without making an effort to read the material that should answer your questions, is the reason you are “singled out.” Likewise, unlike many other commentors, you have major concerns about how the experiment was performed, and thus should have greater reason to read the original paper.

Finally, I realize you are not trying for a PhD. However, you are attempting to discuss a complex topic in science, and seem to want to continue discussing and debating this topic. Your apparent unwillingness to learn about the topic, then, makes your arguments seem hollow, as if you are merely here to repeat the same rhetoric, demanding answers to questions while refusing to acknowledge attempts to answer them, claiming that unless the answer is from the original researcher, the answers are meaningless.

Larry Fafarman
June 16, 2008

Cynthia Wood:

. . .what a gray and impoverished world we would live in if education were limited to only the practical.

So now you are using King Lear’s “O, reason not the need” argument. Ironically, I used the same argument in answering questions about why I “need” to get answers to my questions about the research.

O reason not the need!
Our basest beggars
Are in the poorest thing superfluous.
Allow not nature more than nature needs,
Man’s life is as cheap as beast’s.
Thou art a lady: If only to go warm were gorgeous,
Why, nature needs not what thou gorgeous wear’st,
Which scarcely keeps thee warm.

Larry Fafarman
June 16, 2008

BTW, I might add that far from being too lazy to read up about the study, I would not be able to ask the questions I have been asking about it had I not spent a lot of time reading up about it.

Hoovooloo
June 16, 2008

Reading up about it, yes, but not reading it, an interesting choice for someone who seems to have many questions about the experiment itself. It also renders your claims that you aren’t reading the PDF’s due to length and loading time suspicious, as you seem to claim to have spent plenty of time looking around for commentary.

trone slothrop
June 16, 2008

No Larry, you are just intellectually lazy. And should be treated accordingly. There is no reason to take you seriously. You are not interested in scholarship or actual research.

tyrone slothrop
June 16, 2008

Larry,

Judging from you blog and most recent post, it also appears you are not just intellectually lazy, you are also intellectually dishonest. Zachary’s mistake was to give you the benefit of the doubt. You were never an honest interlocutor.

Larry Fafarman
June 16, 2008

Slothrop barfed,

Zachary’s mistake was to give you the benefit of the doubt.

Zachary never gave me the benefit of anything, dunghill. Just look at all the crap I get when I ask some fair questions.

“So I’m the bad guy. How did that happen?”
— D-Fens in “Falling Down”

Larry Fafarman
June 16, 2008

Hoovooloo said,

First of all, you seem to question if seeing Cit+ was a goal of this experiment, and if so, it would invalidate the experiment as evidence against Behe.

I never said — and I do not think — that “if . . . Cit+ was a goal of this experiment, . . . it would invalidate the experiment as evidence against Behe.” Anyway, what does this experiment have to do with Behe? This experiment started long before Behe’s ID books were published.

As for what was used to induce the mutations, it would seem the experimenters did nothing.

I was not asking about what the experimenters did to induce the mutations — I was only asking if (1) a purpose — or one of the purposes — of the experiment was to evolve citrate-eating bacteria and (2) if the insufficiency of the glucose was intended to give an advantage to citrate-eating bacteria.

Since the experimenters did nothing to directly manipulate the evolution of the bacteria

The environment of lots of citrate and insufficient glucose does give the appearance of an attempt to manipulate the evolution of the bacteria by giving citrate-eating bacteria an advantage over the bacteria that can eat only glucose.

On the note of reading papers, you seem to want a paper that answers, on a single page, these questions that you call basic.

No, I just want direct and consistent answers to simple, basic questions. If a co-author of the paper refuses to answer those questions, then why should I be interested in reading the paper?

I have been sent on wild goose chases through the literature before, where I was told that a particular article had the answers to my questions and I found nothing.

The Internet has several reviews and hundreds of comments about the paper. There is plenty to read without ever looking at the paper.

tyrone slothrop
June 17, 2008

Larry,

You are dishonest.

Larry Fafarman
June 17, 2008

How so?

Hoovooloo
June 17, 2008

I will admit I do not know how to insert quotes into comments, so I will be just using quotation marks.

Larry said:
“I never said — and I do not think — that “if . . . Cit+ was a goal of this experiment, . . . it would invalidate the experiment as evidence against Behe.” Anyway, what does this experiment have to do with Behe? This experiment started long before Behe’s ID books were published” You also say, “I said, ‘This paper is being used to attack the ideas of Michael Behe.'”
Seeing as you already admitted to agreeing with Behe, and accuse us of “attacking” his ideas, it would seem that you are trying to show that the paper does not, in fact, contradict Behe. I’m sorry if I erroneously assumed that your questions relate to your apparent goal/belief, but in light of the fact you seem unwilling to educate yourself, there are few other possible reasons for your questions.

“The environment of lots of citrate and insufficient glucose does give the appearance of an attempt to manipulate the evolution of the bacteria by giving citrate-eating bacteria an advantage over the bacteria that can eat only glucose.”

Indeed it does–that is, after all, how evolution works in nature. However, you seem to have missed the point of my post (which was stated in the sentence following the one you quoted) — that the experimenters did nothing beyond what might occur in nature. Thus, even if their goal was to evolve Cit+ bacteria, the situation they created was not remarkable and their response to that question would have no bearing on interpreting the results of the experiment in terms of the evolution of complex traits.

“I have been sent on wild goose chases through the literature before, where I was told that a particular article had the answers to my questions and I found nothing.”

So because you have had a bad experience with a paper in the past, you refuse to look at the papers that the researcher stated would answer your questions? Did you ever consider that the full answer to your questions might not be as basic as you make them out to be? That it might, indeed, require you to read several pages to fully comprehend? This is why people believe you are unwilling to learn and are intellectually lazy – you refuse to invest the time to actually learn the subject you are attempting to debate, instead relying on second and third-degree conclusions from sources that hardly appear scientific (more on that next).

“The Internet has several reviews and hundreds of comments about the paper. There is plenty to read without ever looking at the paper.”

Yes, I looked at one of the websites you linked to earlier. What was the url, creationontheweb? Certainly sounds like a reasonable, unbiased, scientifically literate source for information. It was also the source you drew upon as contradicting some of the statements made by the researchers and commenters on this blog. That’s intellectual honesty at its finest, isn’t it?

Finally, you seem obsessed with having Zachary answer your questions, and claim that his not doing so causes the paper to loose credibility (again, without having read it). As I have said, you seem, from your written statements, to already believe that Behe is correct, and are looking for ways to prove the paper’s conclusions wrong. Since you have not actually read the paper, this is what we call a “bias” — defined by Princeton as “a partiality that prevents objective consideration of an issue or situation.” Thus, I must ask you, why should Zachary respond to you? You refuse to read the material he provided you with to answer your questions, you appear biased against his conclusions, and refuse to listen to others who are trying to help you understand. If I was Zachary, I certainly wouldn’t be hanging on your every word in the comments section of some blog.

tyrone slothrop
June 17, 2008

Larry,

Your question is dishonest in the sense that it is not a sincere question and you are dishonest in the sense that you do not tell the truth. Now, go read your comments and your blog and note all the dishonest statements that you have made.

Larry Fafarman
June 17, 2008

Here we go again.

Hoovooloo said,

it would seem that you are trying to show that the paper does not, in fact, contradict Behe.

At this point I am not trying to show anything — I am trying to get answers to some simple, basic questions.

Zachary could answer my questions in at most a few sentences or even with just a yes or no answer, or he could refer me to specific pages in the literature where my questions are answered — instead he just vaguely refers me to a lot of literature. I am trying to find out what parts of the experimental results were planned for, or anticipated, or hoped for, or wished for, or longed for, or whatever, and what parts of the results were unanticipated, or completely unexpected, or lucky, or serendipitous, or what have you. Those things are fundamental to my ability to understand the experiment and this paper.

I tried to find out from Zachary whether this experiment was purposely set up to help promote the evolution of Cit+ mutants by giving the bacteria populations insufficient glucose supplies, and he refused to answer. And he has been giving contradictory statements about whether promoting evolution of Cit+ bacteria was a purpose or one of the purposes of the experiment. Even supposing that the questions are unimportant, I still deserve direct and consistent answers. If Zachary does not answer supposedly unimportant questions, why would I think that he would answer important ones?

. . .you seem to have missed the point of my post (which was stated in the sentence following the one you quoted) — that the experimenters did nothing beyond what might occur in nature.

I disagree — the conditions of this experiment could not occur in nature. In this experiment, there was daily cycling of glucose feeding and starvation of the same strains of glucose-eating-only (initially) E. Coli bacteria in a citrate-rich medium over 20 years. I presume that reproduction of the glucose-eating-only bacteria stops when the glucose supply is exhausted in the afternoon (the populations started growing in the morning). It appears that the cycling of glucose feeding and starvation had the following effects:

(1) — it gave the same strains of bacteria repeated opportunities to have preliminary “silent” Cit+ mutations (by “silent” I mean not causing visible effects, such as the mutation that apparently occurred at around 20,000 generations), and —

(2) — at the same time it gave the same strains of bacteria repeated opportunities to have following Cit+ mutations that are expressed (such as the mutation that apparently occurred at around 31,500 generations) and gave these expressed mutations an advantage because bacteria possessing them could feed on the citrate after the glucose supply is exhausted.

Yes, I looked at one of the websites you linked to earlier. What was the url, creationontheweb? Certainly sounds like a reasonable, unbiased, scientifically literate source for information. It was also the source you drew upon as contradicting some of the statements made by the researchers and commenters on this blog.

I did not originally get my ideas there — I was just showing that others got the same impression that I got. And Zachary contradicts himself — he does not need others to contradict him.

tyrone slothrop:

Your question is dishonest in the sense that it is not a sincere question and you are dishonest in the sense that you do not tell the truth.

Wrong. Show me one example of an insincere question from me or where I have not told the truth.

tyrone slothrop
June 17, 2008

Larry,

Thank you for providing more evidence of your intellectual dishonesty. Perhaps, if you did not combine intellectual laziness with intellectual dishonesty, people would not think so little of you.

Now, go back and read all your comments here and your blog and take note of all the dishonest statements that you have made.

Larry Fafarman
June 17, 2008

Larry,
Now, go back and read all your comments here and your blog and take note of all the dishonest statements that you have made.

I asked you to point out specific examples, dunghill. If you can’t, then you are just a big bag of hot air.

Larry Fafarman
June 17, 2008

I broke down and did something I should not have bothered doing — I browsed through the paper. The paper does not explicitly state — but definitely gives the impression — that observing evolution of Cit+ E. coli mutants was a purpose if not the sole purpose of the experiment (some other reasons for the experiment have been given here). Then Zachary created confusion here by making contradictory statements about whether evolving Cit+ mutants was a goal of the experiment. What kind of credibility does he think he has?

“So I’m the bad guy. How did that happen?”
— D-Fens in “Falling Down”

tyrone slothrop
June 17, 2008

Larry,

I told you to go back and read your comments and blog and find all the places where you have been dishonest. I believe it might be useful for you. You have not done that yet and have instead begun again asking for someone else to do all the work. You are lazy. Post #196 is an example of your laziness again.

I also pointed out that your post #194 is an example of both your dishonesty and your intellectual laziness. Read it again and note all the places you were less than honest.

Now, considering that you have a proven track record of dishonesty and laziness, you will forgive me if your opinion of me seems irrelevant.

Hoovooloo
June 17, 2008

Here we go again.

“I am trying to get answers to some simple, basic questions.”

And you did, in the form of a series of papers that were referred to you. Your unwillingness to read them is why I believe you are unwilling to learn. You claim to have been sent on “wild goose chases” before. However, if your goal truly is to learn, you would have accepted, perhaps appreciated, the chance to dig deeper into the subject, albeit unintentionally. That you reject the papers for fear of this happening, directly contradicts your assertion of being willing to learn.

“I still deserve direct and consistent answers. If Zachary does not answer supposedly unimportant questions, why would I think that he would answer important ones?”

1) Why do you deserve answers? Especially since you have already stated you believe Behe, and thus that you disagree with the conclusion of the paper, you do not appear to simply be trying to educate yourself, or else you should approach this with an open mind.

2) He would answer the important questions because they are important. If the question is unimportant, asserting that you deserve an answer to it implies that you believe you are more important than most other things he has to do — arrogant at best, delusional at worst.

“I disagree — the conditions of this experiment could not occur in nature. In this experiment, there was daily cycling of glucose feeding and starvation of the same strains of glucose-eating-only (initially) E. Coli bacteria in a citrate-rich medium over 20 years.”

This statement shows a remarkable disregard for how the world works. From day/light cycles, to the tides, to waves, to circadian rhythm, to seasons, the world is periodic. In the event of food appearing/disappearing over the course of a day, consider photosynthesis — it will only be producing food during the day. Or sap dripping from a tree. Or animals defecating at somewhat regular intervals. Or a bacteria that lives in the mouth/ stomach of an animal that feeds once or twice a day. These are all situations where a bacteria could see a sudden periodic influx of one type of food, and an accumulation of another (unusable) type of potential food over a period of time. Now, I do not know enough about bacteria to say any specific examples where E. Coli has an abundance of citrate and a periodic influx of glucose, but these are all situations, that could occur in nature, where you see a periodic influx of food, directly contradicting your statement.

“(1) — it gave the same strains of bacteria repeated opportunities to have preliminary “silent” Cit+ mutations (by “silent” I mean not causing visible effects, such as the mutation that apparently occurred at around 20,000 generations), and –”

If the mutation does not cause any visible effect, the offspring with it would have been just as well suited as their neighbors, thus the mutation could have existed and propagated even if there were an abundance of glucose (see genetic drift).

“(2) — at the same time it gave the same strains of bacteria repeated opportunities to have following Cit+ mutations that are expressed (such as the mutation that apparently occurred at around 31,500 generations) and gave these expressed mutations an advantage because bacteria possessing them could feed on the citrate after the glucose supply is exhausted.”

Any successful mutation will give the bacteria in question an advantage in the given environment. I fail to see how the bacteria adapting to environment might somehow invalidate the conclusions of the experiment.

“I did not originally get my ideas there — I was just showing that others got the same impression that I got. And Zachary contradicts himself — he does not need others to contradict him.”

Then where did you get your ideas? After all, you did not read the paper. Also, your so-called contradiction is, in fact, not:

“When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit
— and —
the intent of the experiment was never to evolve a Cit+ E. coli variant”

Note that the first part refers to Dr. Lenski, while the second refers to the design of the experiment, and thus the first part does not directly imply anything about the experimental setup. In addition, Dr. Lenski said the bacteria might OR might not take advantage of the opportunity. Thus, the evolution of Cit+ was seen as a possibility, not a goal.

Hoovooloo
June 18, 2008

I too, read the paper (I notice you used “browsed” instead of “read” — how deep was this browsing?) and it seemed to confirm that Cit+ was not the goal for the experiment. The goal of the experiment was to test if evolution was mostly random, or if natural selection would lead to highly similar results if you “re-played” history. That was the goal of the experiment — Cit+ was merely one of many possible outcomes that could be used to test the starting hypothesis. Thus, while the environment was particularly well-suited to Cit+ bacteria, it would be disingenuous to claim that Cit+ was a goal of the experiment. In addition, as I have already said, it is necessary to put E. coli in an environment to which it is not well-suited in order to produce any noticeable effects of evolution. Thus, the citrate was a necessary step in this experiment, and the fact that it may lead to Cit+ bacteria was an obvious side effect. However, as I have previously described, situations like this can occur in nature, and thus the addition of the citrate has little effect on the relevancy of the results of the experiments.

Secondly, the fact that you claim you did something you “should not have bothered doing — I browsed through the paper,” further refutes your claim that you are just trying to educate yourself. Had you been interested in educating yourself, you would not claim that you “should not have bothered” actually educating yourself by reading the paper.

Larry Fafarman
June 18, 2008

Hoovoodoo said,

Your unwillingness to read them is why I believe you are unwilling to learn.

Will you stop that “unwilling to learn” crap? I have spent a hell of a lot of time trying to learn what is going on here.

Why do you deserve answers?

Because I deserve them.

Especially since you have already stated you believe Behe, and thus that you disagree with the conclusion of the paper

I don’t see how Behe’s statements are in conflict with the conclusion of the paper.

If the question is unimportant, asserting that you deserve an answer to it implies that you believe you are more important than most other things he has to do

It’s not just a matter of whether my questions are “important.” Zachary has been making some mutually contradictory statements here and contradicting common sense about the purposes of the experiment.

the world is periodic. In the event of food appearing/disappearing over the course of a day, consider photosynthesis — it will only be producing food during the day. Or sap dripping from a tree. Or animals defecating at somewhat regular intervals. Or a bacteria that lives in the mouth/ stomach of an animal that feeds once or twice a day.

The variations in those things do not necessarily result in variations in the environments of bacteria.

I do not know enough about bacteria to say any specific examples where E. Coli has an abundance of citrate and a periodic influx of glucose, but these are all situations, that could occur in nature, where you see a periodic influx of food, directly contradicting your statement.

This experiment is closely controlled and could not occur in nature. There are twelve lines of bacteria from a single individual. The lines of bacteria are protected from contamination. The bacteria constantly live in a citrate-rich environment. They are given a fixed insufficient supply of glucose every day. The experiment has been going on for 20 years.

If the mutation does not cause any visible effect, the offspring with it would have been just as well suited as their neighbors, thus the mutation could have existed and propagated even if there were an abundance of glucose

That’s true — but that “silent” mutation would give no advantage to those bacteria in comparison to their neighbors. But a lack of glucose gives an advantage to bacteria with mutations that do have a “visible” effect — i.e., that give the ability to eat citrate — because those bacteria can continue propagating while their neighbors cannot.

Any successful mutation will give the bacteria in question an advantage in the given environment.

I don’t know what you mean by “successful” mutation — a mutation enabling bacteria to breed faster, for example, will give an advantage. But I am specifically talking here about the ability to eat citrate.

I fail to see how the bacteria adapting to environment might somehow invalidate the conclusions of the experiment.

I never made the absurd claim that the adaptation of bacteria to their environment might somehow invalidate the conclusions of the experiment. You are putting all kinds of words in my mouth.

Then where did you get your ideas? After all, you did not read the paper.

I got my ideas from where most commenters got their ideas — from the descriptions of the experiment and the paper.

Note that the first part refers to Dr. Lenski, while the second refers to the design of the experiment, and thus the first part does not directly imply anything about the experimental setup.

Sheeeesh — didn’t Dr. Lenski design the experiment?

the evolution of Cit+ was seen as a possibility, not a goal.

If Cit+ evolution was seen as a possible and desirable outcome, then by definition it was a goal. Goals don’t have to be sure outcomes.

I too, read the paper (I notice you used “browsed” instead of “read” — how deep was this browsing?)

Deep enough.

and it seemed to confirm that Cit+ was not the goal for the experiment.

What other goals of the experiment does the paper mention?

while the environment was particularly well-suited to Cit+ bacteria, it would be disingenuous to claim that Cit+ was a goal of the experiment.

As I said, if Cit+ evolution was seen as a possible and desirable outcome, then by definition it was a goal.

However, as I have previously described, situations like this can occur in nature

The conditions of this experiment could at most only be very crudely and very inefficiently reproduced in nature, if at all.

the fact that you claim you did something you “should not have bothered doing — I browsed through the paper,” further refutes your claim that you are just trying to educate yourself.

I said that I “should not have bothered” because I am rightly very pissed off that my questions are not being answered here.

Anyway, you are wasting your time trying to protect Zachary from the loss of credibility resulting from his mutually contradictory and nonsensical statements and his refusal to answer some simple, basic questions here.

Hoovooloo
June 18, 2008

And again.

“Because I deserve them”

Well that’s a reasonable answer, isn’t it? But your unwillingness to work for these answers through research (reading the other papers, perhaps?), instead demanding the answers be spoon-fed to you is why people consider you intellectually lazy. You also seem to have missed why I consider you unwilling to truly learn:

“‘I am trying to get answers to some simple, basic questions.’

And you did, in the form of a series of papers that were referred to you. Your unwillingness to read them is why I believe you are unwilling to learn. You claim to have been sent on “wild goose chases” before. However, if your goal truly is to learn, you would have accepted, perhaps appreciated, the chance to dig deeper into the subject, albeit unintentionally. That you reject the papers for fear of this happening, directly contradicts your assertion of being willing to learn.”

“I don’t see how Behe’s statements are in conflict with the conclusion of the paper.”

If you cannot see how the claim that “If two mutations have to occur before there is a net beneficial effect — if an intermediate state is harmful, or less fit than the starting state — then there is already a big evolutionary problem.” (4) And what if more than two are needed? The task quickly gets out of reach of random mutation” (extracted from your comment [19] on the follow-up post) contradicts the conclusion in the paper that one strain required at least three mutations to evolve Cit+, including one mutation that was not directly beneficial, then not only are you unwilling to learn, you are deluding yourself so that there is no hope in actually trying to discuss this issue with you. Unless, of course, you are trying to show that the conclusions of the paper are wrong, in which case you would have been lying when you previously denied that. Oh, and I realize Behe never claims that it is impossible, just that it would be incredibly difficult. However, these mutations occurred in ~20 years which, given the billions of years evolution has to work, would again seem to refute Behe.

“It’s not just a matter of whether my questions are “important.” Zachary has been making some mutually contradictory statements here and contradicting common sense about the purposes of the experiment.”

Interesting that you suddenly change the reason for denying his credibility from his “unwillingness” to answer unimportant questions to his “contradicting common sense.” I have only seen the one “contradicting” comment, and I have already stated why it does not contradict itself (I will respond to your points about that later). Also, science often contradicts common sense — just look at quantum mechanics — so that point of contention is meaningless.

“The variations in those things do not necessarily result in variations in the environments of bacteria.”
–and–
“This experiment is closely controlled and could not occur in nature. There are twelve lines of bacteria from a single individual. The lines of bacteria are protected from contamination. The bacteria constantly live in a citrate-rich environment. They are given a fixed insufficient supply of glucose every day. The experiment has been going on for 20 years.”

Can you honestly say that? Do you know the details of every biological process, every potential habitat for E. coli? Can you also show that the experiment was so wildly dislike nature that it is meaningless, as you seem to imply? In addition, you have not actually refuted any of my examples, simply dismissing them by saying that the cycles of food availability may not match the cyclical processes I mentioned. While that may be true, neither of us really know if this sort of environment is impossible, and thus arguing this point is useless. That leaves your point about contamination. If you knew anything about evolution, you would know that increasing competition will increase the selection pressures, effectively increasing evolution. So, eliminating contamination may have been beneficial OR detrimental. Again, until someone here can prove which one it was, arguing the point is useless.

“That’s true — but that “silent” mutation would give no advantage to those bacteria in comparison to their neighbors. But a lack of glucose gives an advantage to bacteria with mutations that do have a “visible” effect — i.e., that give the ability to eat citrate — because those bacteria can continue propagating while their neighbors cannot.”

That is indeed true — bravo. However, you seem to have failed to realize that my comment was a response to your comment, that the glucose-cycling “gave the same strains of bacteria repeated opportunities to have preliminary “silent” Cit+ mutations (by “silent” I mean not causing visible effects, such as the mutation that apparently occurred at around 20,000 generations),” which you seemed to use as a reason why the glucose-cycling was poor experimental set-up. That you now agree with me that the “silent” mutations would not affect their survival relative to neighbors regardless of the glucose cycling, contradicts your earlier statement. If you have learned enough about science to have changed your mind, excellent.

“I don’t know what you mean by “successful” mutation — a mutation enabling bacteria to breed faster, for example, will give an advantage. But I am specifically talking here about the ability to eat citrate.”
–and–
“I never made the absurd claim that the adaptation of bacteria to their environment might somehow invalidate the conclusions of the experiment. You are putting all kinds of words in my mouth.”

What is your point? You repeated say you are not trying to show that the paper has drawn incorrect conclusions or that the experiment was designed wrong, yet every question you ask, every post you link to, every comment you make seems to serve one of those purposes. Do not claim that your purpose is simply self-education, as I have provided ample evidence where your actions or comments contradict this goal. Again, I apologize if the goal I assumed you had based on your past posts was incorrect. I feel, however, the only way to continue this discussion is for you to clarify what point you are trying to make.

“What other goals of the experiment does the paper mention?”
— and —
“If Cit+ evolution was seen as a possible and desirable outcome, then by definition it was a goal. Goals don’t have to be sure outcomes.”

Please show me where Dr. Lenski or the paper claimed that Cit+ had been seen, in advance, as a desirable outcome. It was certainly seen as a possibility, but did any of them state that they wanted to see Cit+ evolve (not IF Cit+ would evolve, but that they specifically wanted it to happen)? Retroactively viewing Cit+ evolution as desirable does not count, as it it was not considered desirable at the start of the experiment, it cannot truly be called a goal of the experiment. If you cannot find such a direct quote, then you are projecting your own biases and beliefs onto the research, thus furthering claims of intellectual dishonesty.

“The conditions of this experiment could at most only be very crudely and very inefficiently reproduced in nature, if at all.”

Again, prove it. You are making a bold claim about poor experimental set-up, without any evidence to back you up. In addition, why does it matter if the situation could only be replicated “crudely”? It would still be a valid experiment (depending on how closely it replicated nature). In addition, remember, lack of evidence for one side is generally not evidence for the other, so my not having proved it was a valid set-up does not make it an invalid one..

“I said that I “should not have bothered” because I am rightly very pissed off that my questions are not being answered here.

Anyway, you are wasting your time trying to protect Zachary from the loss of credibility resulting from his mutually contradictory and nonsensical statements and his refusal to answer some simple, basic questions here.”

Again, how does a researcher not answering the self-described basic and unimportant questions of someone who appears biased and refuses to read the material the researcher has provided them to answer their question make you “rightly pissed?” Unless, of course, you have some sort of superiority complex or delusion of grandeur.

In addition, you seem to be the only one that doubts Zachary’s credibility. I am not here to “defend” it, rather to try to demonstrate to you where your logic has gone awry and teach you about evolution, a chance that someone who claims they are interested in learning should jump on.

LFP
June 18, 2008

By now, after 200 comments, I hope everybody has learned a valuable lesson: it’s a waste of time to argue with creationists and other “true believers.” The only way to combat scientific illiteracy in the US is to massively revamp middle and high school science education. Creationists, by definition, have closed minds, so argument has no effect. That’s the very nature of dogmatic, magical thinking. It’s going to take a “Marshall Plan” for schools, and generations of time, to reduce the incidence of Larry-style ignorance.

By the way, you all do know that Larry is also a Holocaust denier, right? That’s the bottom rung of extreme kookery. Let’s move on, shall we?

Ale
June 18, 2008

I see nothing contradictory in the way the experiment was set up, nor in the intentions of the experimenters, nor on its conclusions. My opinion on them is extremely high: their work is one of the clearest examples of good science I have seen. Their credibility is as high as it can be. Fafarman’s credibility, though, is in the gutter: well-intentioned commenters have answered his questions many times, and yet he persists presenting the exact same views. It is clear that his beliefs are uncorrelated with evidence.

Rob
June 18, 2008

a creationist and a holocaust denier to boot – thats too good to be true. and all hiding behind his banner of ‘skepticism’ – as if skepticism is about taking a contrarian world view instead of an evidence based approach. What a joke of a human being

Larry Fafarman
June 18, 2008

Hoovooloo driveled,

And you did, in the form of a series of papers that were referred to you.

Answering specific questions by referring me to a big stack of literature is not acceptable. It is called “bibliography bluffing.”

If you cannot see how the claim that “If two mutations have to occur before there is a net beneficial effect — if an intermediate state is harmful, or less fit than the starting state — then there is already a big evolutionary problem.”

I should not have included the following Behe quote: “if an intermediate state is harmful, or less fit than the starting state.” It is irrelevant here, and I think that Behe included it only because he was quoting a previous work of his. I should have just quoted Behe as saying, “If two mutations have to occur before there is a net beneficial effect . . . . then there is already a big evolutionary problem.”

contradicts the conclusion in the paper that one strain required at least three mutations to evolve Cit+,

Where was the 3rd required mutation? There apparently was a mutation at around 20,000 generations and then another mutation at around 31,500 generations, and then the Cit+ bacteria increased from 0.5% of the population to 19% at 33,000 generations and then nearly disappeared before starting to grow again in numbers and becoming predominant. I have seen no explanation for the near-disappearance of the Cit+ bacteria.

However, these mutations occurred in ~20 years which, given the billions of years evolution has to work, would again seem to refute Behe

These mutations were very simple — this was just microevolution — and the E. coli bacteria were almost ready to utilize citrate. Michael Behe said,

. . wild E. coli already has a number of enzymes that normally use citrate and can digest it (it?s not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a “citrate permease” which can transport citrate from outside the cell through the cell’s membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, “The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.”

Hoovooloo said,

Interesting that you suddenly change the reason for denying his credibility from his “unwillingness” to answer unimportant questions to his “contradicting common sense.”

I didn’t change anything, I was just giving different reasons for denying his credibility. Actually, his statements contradicting common sense were part of his unwillingness to answer questions. And I don’t consider my questions to be unimportant.

“This experiment is closely controlled and could not occur in nature. There are twelve lines of bacteria from a single individual. The lines of bacteria are protected from contamination. The bacteria constantly live in a citrate-rich environment. They are given a fixed insufficient supply of glucose every day. The experiment has been going on for 20 years.”

Can you honestly say that? Do you know the details of every biological process, every potential habitat for E. coli?

Can you “honestly” say that those conditions are likely to occur in nature?

. . .which you seemed to use as a reason why the glucose-cycling was poor experimental set-up.

I never said, and I don’t think, that the glucose-cycling was poor experimental set-up. You keep making these straw man arguments misrepresenting what I actually say.

That you now agree with me that the “silent” mutations would not affect their survival relative to neighbors regardless of the glucose cycling, contradicts your earlier statement.

The apparent purpose of the glucose cycling was to give an advantage to citrate-eating bacteria while giving the glucose-eating-only bacteria continuing opportunities to have mutations during reproduction.

You repeated say you are not trying to show that the paper has drawn incorrect conclusions or that the experiment was designed wrong, yet every question you ask, every post you link to, every comment you make seems to serve one of those purposes.

I never said or implied here that I think that the paper has drawn incorrect conclusions. I do have some criticisms about the way the experiment was designed, but I don’t think that the design is completely wrong.

It is Zachary who created confusion in this comment thread by making mutually contradictory and nonsensical statements about the purposes of the experiment. Until he made those statements, I thought that I understood the experiment.

LFP barfed,

By the way, you all do know that Larry is also a Holocaust denier, right?

I am a holocaust revisionist, not a holocaust denier, dunghill. And that is just an ad hominem attack. All that counts here are the statements that I make here.

Ale said,

I see nothing contradictory in the way the experiment was set up, nor in the intentions of the experimenters, nor on its conclusions.

Wrong — Zachary made contradictory statements here about the intentions of the experimenters.

Rob barfed,

a creationist and a holocaust denier

I’m not a creationist either, dunghill.

John Morales
June 19, 2008

To Larry, “All that counts here are the statements that I make here”: You’ve been allowed exceptional latitude to make your opinions known.

My opinion, based on what you’ve said here, and especially the way you’ve said it, is that you are obnoxious and are attempting to insinuate (but failing to) that the experiment is somehow flawed.

Preemptively, I note that I am typing this, not drivelling or barfing.

To Carl, may I say your blog is excellent and informative, and that I am amazed at the latitude you allow commenters.

Larry Fafarman
June 19, 2008

John Immorales moaned,

To Larry, “All that counts here are the statements that I make here”: You’ve been allowed exceptional latitude to make your opinions known.

Where’s the “latitude”? All of my comments here have been on-topic, serious, and — until other started insulting me — polite.

My opinion, based on what you’ve said here, and especially the way you’ve said it, is that you are obnoxious and are attempting to insinuate (but failing to) that the experiment is somehow flawed.

So? What is wrong with criticizing the experiment? Anyway, most of my comments have not criticized the experiment.

I am amazed at the latitude you allow commenters.

And I am amazed at your asininity.

It is understandable that Carl would not want to develop a bad reputation for arbitrarily censoring comments.

Idiot.

Hoovooloo
June 19, 2008

“Hoovooloo driveled”

I “driveled” now, did I? Glad to see we’re keeping a high level of discourse.

“Answering specific questions by referring me to a big stack of literature is not acceptable. It is called “bibliography bluffing.””

Unless of course, the “big stack” (two whole papers, lord have mercy!) actually answers you questions. Of course, you don’t know if it is “bibliography bluffing,” as you refuse to read them.

“I should not have included the following Behe quote: “if an intermediate state is harmful, or less fit than the starting state.” It is irrelevant here, and I think that Behe included it only because he was quoting a previous work of his. I should have just quoted Behe as saying, “If two mutations have to occur before there is a net beneficial effect . . . . then there is already a big evolutionary problem.””

Okay, but my point still stands. Behe said that having two mutations, one of which is silent (confers no immediate advantage) would be a “big evolutionary problem.” Of course, at least two mutations did occur, one of which was silent, in a scale of 20 years, again refuting Behe.

“Where was the 3rd required mutation? There apparently was a mutation at around 20,000 generations and then another mutation at around 31,500 generations, and then the Cit+ bacteria increased from 0.5% of the population to 19% at 33,000 generations and then nearly disappeared before starting to grow again in numbers and becoming predominant. I have seen no explanation for the near-disappearance of the Cit+ bacteria.”

From near the top of the second column on page 6 of the paper, “At least one mutation in the LTEE was necessary to produce a genetic background with the potential to generate Cit variants, while the distribution and dynamics of Cit mutants in fluctuation tests indicate at least two additional mutations are involved.” 1+2=3. Clearly your reading of the paper was not “deep enough.”

“These mutations were very simple — this was just microevolution”

Macroevolution is evolution that causes speciation, as defined by carm.org, an organization that, if anything, would be biased to have more difficult qualifications for macroevolution. As has been stated numerous times, Cit- is a defining feature of E. coli that is often used to identify E. coli as a species. Since the line of speciation is blurred at the bacterial level anyway, this was not “just microevolution.” Again, this demonstrates your lack of knowledge in this discussion.

“and the E. coli bacteria were almost ready to utilize citrate”

Meaningless statement. Unless you have some reasonable means to quantify “almost ready,” you can claim anything is “almost ready” to evolve any other feature. I can claim that, since bacteria already have the basic mechanisms for reproduction in place, they are “almost ready” to evolve sexual reproduction–they already have half the steps working.

“I didn’t change anything, I was just giving different reasons for denying his credibility. Actually, his statements contradicting common sense were part of his unwillingness to answer questions. And I don’t consider my questions to be unimportant.”

You still haven’t provided me with those direct quotes where Cit+ was a goal of the experiment, and thus lack evidence for claims of Zachary’s contradictions. Likewise, as I already pointed out, science contradicting common sense is not sufficient reason for denying someone’s credibility, as quantum mechanics shows. You were the one that called your questions unimportant previously, when you stated that Zachary refuses to answer the unimportant questions.

“Can you “honestly” say that those conditions are likely to occur in nature?”

No, as I clearly stated. However, I am not the one in disagreement with the people who should know if these situations are naturally possible. That you claim they are not, yet provide no evidence to support your claim, is why I consider your claim not to be credible. Remember, appeals to authority are only invalid if the expert is not truly qualified or failed to apply their expertise.

“I never said, and I don’t think, that the glucose-cycling was poor experimental set-up. You keep making these straw man arguments misrepresenting what I actually say. ”
–and–
“I never said or implied here that I think that the paper has drawn incorrect conclusions. I do have some criticisms about the way the experiment was designed, but I don’t think that the design is completely wrong.”

The criticisms and questions you have made against the experimental set-up itself have almost exclusively focused on glucose-cycling and if Cit+ was a goal. You state that you have criticisms about the design, then focus your comments on glucose cycling, going so far as to list ways it may have influenced the experiment. Again, this would imply that one of your criticisms is, in fact, the glucose cycling., Since it isn’t, please do tell us your criticisms.

In addition, you have stated that you agree with Behe, and I and others have shown that Behe’s beliefs are in direct conflict with the conclusions drawn in the paper. Thus, at some level, you must either disagree with the paper, or be delusional.

“The apparent purpose of the glucose cycling was to give an advantage to citrate-eating bacteria while giving the glucose-eating-only bacteria continuing opportunities to have mutations during reproduction.”

No, the apparent purpose of the cycling was to provide an environment to which E. coli is not naturally well-suited, to increase selective pressure, not specifically to evolve Cit+ bacteria. Dr. Lenski’s quote supports this, as he states that it may be a point of divergence.

“It is Zachary who created confusion in this comment thread by making mutually contradictory and nonsensical statements about the purposes of the experiment. Until he made those statements, I thought that I understood the experiment.”

You are the only one here that appears confused. Is it more reasonable, then, to attribute this to Zachary, or to your own biases and misunderstandings? I’m gonna go with the latter.

“Wrong — Zachary made contradictory statements here about the intentions of the experimenters.”

No, he didn’t, and until you provide me with those quotes I requested, you have no evidence for your position. Oh, and saying “go back and look at the paper,” as you did to me when I requested those quotes, is exactly the same intellectual sin you accuse Zachary of having committed, another case of intellectual dishonesty.

“I’m not a creationist either, dunghill.”

As eloquent a response as I’ve come to expect from you.

Finally, you have contradicted yourself. Look here:
“It appears that the cycling of glucose feeding and starvation had the following effects:
(1) — it gave the same strains of bacteria repeated opportunities to have preliminary “silent” Cit+ mutations (by “silent” I mean not causing visible effects, such as the mutation that apparently occurred at around 20,000 generations),” (post 194)
–and–
“That’s true — but that “silent” mutation would give no advantage to those bacteria in comparison to their neighbors. But a lack of glucose gives an advantage to bacteria with mutations that do have a “visible” effect — i.e., that give the ability to eat citrate — because those bacteria can continue propagating while their neighbors cannot.” (post 201)

In post 201, you agree that silent mutations would be unaffected by the food source. In post 194, however, you claim that the glucose cycling would have the effect of allowing silent mutations. You have contradicted yourself in how glucose cycling would effect the silent mutations and thus, following your own logic, you have lost the small credibility you had left.

Larry Fafarman
June 19, 2008

Hoovooloo said,

I “driveled” now, did I? Glad to see we’re keeping a high level of discourse.

Just one of those papers, the subject of this post, has eight pages of fine print.

Behe said that having two mutations, one of which is silent (confers no immediate advantage) would be a “big evolutionary problem.” Of course, at least two mutations did occur, one of which was silent, in a scale of 20 years, again refuting Behe.

Even the first mutation was a big evolutionary problem — it occurred in only one of 12 lines of bacteria in 20 years. And it was not a particularly big mutation.

“Where was the 3rd required mutation?

From near the top of the second column on page 6 of the paper, “At least one mutation in the LTEE was necessary to produce a genetic background with the potential to generate Cit variants, while the distribution and dynamics of Cit mutants in fluctuation tests indicate at least two additional mutations are involved.” 1+2=3. Clearly your reading of the paper was not “deep enough.”

That was just one little statement in eight pages of fine print. And it doesn’t answer my question of where the 3rd mutation was.

As has been stated numerous times, Cit- is a defining feature of E. coli that is often used to identify E. coli as a species. Since the line of speciation is blurred at the bacterial level anyway, this was not “just microevolution.”

Yes, the original post says,

If E. coli is defined as a species that can’t eat citrate, does that mean that Lenski’s team has witnessed the origin of a new species? The question is actually murkier than it seems, because the traditional concept of species doesn’t fit bacteria very comfortably.

Since it is not clear that a new species was created (your definition of macroevolution), it is not clearly macroevolution either. Since “e” is the vowel between “a” and “i”, maybe it should be called “mecroevolution.”

Again, this demonstrates your lack of knowledge in this discussion.

No, it just demonstrates your lack of understanding of the fine points of this discussion.

Unless you have some reasonable means to quantify “almost ready,” you can claim anything is “almost ready” to evolve any other feature.

Again, Michael Behe said, “all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there.”

You still haven’t provided me with those direct quotes where Cit+ was a goal of the experiment, and thus lack evidence for claims of Zachary’s contradictions.

Here is a direct quote of Zachary, from comment #115:

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding — I will need to check with him to make certain I understand this properly).

Hoovooloo said,

You were the one that called your questions unimportant previously, when you stated that Zachary refuses to answer the unimportant questions.

No, I called them unimportant only for the sake of argument (“assuming arguendo,” as lawyers say). To me, they are important.

“Can you “honestly” say that those conditions are likely to occur in nature?”
No, as I clearly stated. However, I am not the one in disagreement with the people who should know if these situations are naturally possible.

Has anyone “who should know” said that these situations are naturally possible? If none, then I have not disagreed with them.

The criticisms and questions you have made against the experimental set-up itself have almost exclusively focused on glucose-cycling and if Cit+ was a goal.

I said that it appears that the purpose of the glucose-cycling was to promote the evolution of Cit+ bacteria. Zachary has neither confirmed nor denied that this was the purpose of the glucose-cycling.

In addition, you have stated that you agree with Behe, and I and others have shown that Behe’s beliefs are in direct conflict with the conclusions drawn in the paper.

Where have you or others shown that Behe’s beliefs are in direct conflict with the conclusions drawn in the paper?

No, the apparent purpose of the cycling was to provide an environment to which E. coli is not naturally well-suited, to increase selective pressure, not specifically to evolve Cit+ bacteria.

The purpose or effect of “selective pressure” is promotion of evolution of Cit+ bacteria. You are just playing word games.

Dr. Lenski’s quote supports this, as he states that it may be a point of divergence.

“Divergence” is just a high-falutin term for “evolution.”

You are the only one here that appears confused.

Maybe there are other confused readers here but they just haven’t spoken up.

“Wrong — Zachary made contradictory statements here about the intentions of the experimenters.”
No, he didn’t, and until you provide me with those quotes I requested, you have no evidence for your position.

I provided the quotes in comment #150.

Oh, and saying “go back and look at the paper,” as you did to me when I requested those quotes,

I never asked you to “go back and look at the paper”!

“I’m not a creationist either, dunghill.”
As eloquent a response as I’ve come to expect from you.

My insult was justified by the comment I was responding to.

In post 201, you agree that silent mutations would be unaffected by the food source. In post 194, however, you claim that the glucose cycling would have the effect of allowing silent mutations. You have contradicted yourself in how glucose cycling would effect the silent mutations and thus, following your own logic, you have lost the small credibility you had left.

How can I lose credibility before I even have a chance to clarify my statements?

Actually, the silent mutations were affected by the food source. When there was no glucose and only citrate to consume, the bacteria that could eat only glucose could not reproduce and not being able to reproduce affected silent mutations because (1) mutations are likely to occur during gene duplication in reproduction and (2) reproduction tends to increase the number of mutants (though not rapidly in the case of the silent mutation because the silent mutation gave no advantage).

Giving each population an insufficient glucose supply gives Cit+ bacteria an advantage because they can continue to reproduce after the glucose supply is exhausted.

You are making this look much harder than it actually is.

JKessler
June 19, 2008

Been lurking but I figured I’d agree with the others that there is nothing conflicting in the quotes provided on comment 150.

Possible occurrence > goal.

JKessler
June 19, 2008

Gah, that should read “Possible occurrence does not equal goal”

Larry Fafarman
June 19, 2008

JKessler said,

Been lurking but I figured I’d agree with the others that there is nothing conflicting in the quotes provided on comment 150. Possible occurrence does not equal goal.

I strenuously disagree. Anything foreseen as a possible and desirable outcome is a “goal.” A goal does not have to be a sure outcome. In fact, the word “goal” implies uncertainty. One of my printed dictionary’s definitions of “goal” is “an object or end that one strives to attain.” Note the word “strives,” which only means that there is an effort towards the goal, not that there is certainty that the goal will be attained. The word “strives” means making an effort, and merely conducting the experiment was an effort even if nothing specific was done to try to promote the evolution of Cit+ E. coli. If Cit+ evolution had been a certainty, “purpose” would have been a more appropriate word, as in, “the purpose of the experiment was to observe Cit+ evolution,” but even that could be interpreted as possibly having uncertainty. And “purpose” can be used in a clear context of uncertainty, as in, “the purpose of the experiment was to try to evolve Cit+ E. coli.” Rather than depending on the connotations of words, it is better to somehow clearly indicate (as by the word “try” or some positive statement) that Cit+ evolution was a certainty or Cit+ evolution was not a certainty (anyway, it is clear from the results of the experiment that it was not a certainty).

Also, I asked if the purpose or one of the purposes of the insufficiency of the glucose supply was to try to promote the evolution of Cit+ E. coli, and I got no answer at all from Zachary and no straight answer from others — one commenter just called it an “environmental stressor.” Please — let’s stop playing word games.

Tulse
June 19, 2008

Larry, the E. coli don’t give a damn what the possible “purpose” of the experiment was, and whatever the intent the experimenters had, that doesn’t somehow magically affect DNA. The “purpose” of the study is irrelevant to its outcomes.

Larry Fafarman
June 19, 2008

Tulse,

You are still playing word games. If this experiment had no goal and no purpose, then what in hell did this experiment have?

Hoovooloo
June 19, 2008

“Just look at the insults you make.”

Where? Oh, and calling you intellectually dishonest or lazy is not really an insult if I support my claim with evidence, as I did.

“Just one of those papers, the subject of this post, has eight pages of fine print.”

My god! Eight whole pages of fine print! Is there no justice on this planet? Also, I read that paper in less than 20 minutes, and apparently read it more closely than you did, so I would hardly consider it an extreme amount of literature. Oh, and as you failed to note, the fact that you have not read the other papers, and thus do not know what they say, means you cannot factually state that Zachary was “bibliography bluffing.”

“Even the first mutation was a big evolutionary problem — it occurred in only one of 12 lines of bacteria in 20 years. And it was not a particularly big mutation.”

Yes, but it occurred in

AC
June 19, 2008

I strenuously disagree. Anything foreseen as a possible and desirable outcome is a “goal.”

According to standard definitions and usage of English words, you are, quite simply, incorrect.

People who are not biologists or lawyers can get by quite well without knowing anything about Darwinism or the Constitution (even many biologists do not need to know anything about Darwinism). In fact, I heard of a survey where people were asked to name some freedoms or rights protected by the Bill of Rights, and a large percentage of people could not name a single one — if they had named just one, say, freedom of speech, they would have gotten credit for successfully answering the question. However, people need to know something about arithmetic just to handle money.

This, however, is simply a shame. If you honestly cannot see how it is a grave problem for any citizen of the United States to not know its Constitution (among other things related to its laws and government), then you are yourself a very poor citizen. Furthermore, the idea that people should only be educated in subjects that (painfully) directly relate to their chosen profession is laughable. You would create a nation of overspecialized ignoramuses in the place of flexible, responsible, informed citizens. We are too close to that situation already, sir.

Larry Fafarman
June 19, 2008

Hoovooloo said,

My god! Eight whole pages of fine print!

It’s not a direct answer to very simple questions, bozo!

Yes, but it occurred in

???? What were you going to say?

Yes, but it was one little statement that you missed

It was one little statement in eight pages of fine print and it didn’t even answer my question!

You admit there was a mutation at 20,000, then another at 31,500, and then a population explosion later on. Could the population explosion have been caused by another mutation?

But what caused the Cit+ bacteria to nearly disappear after growing to 19% of the population? Was that the result of a mutation? And maybe there was a fourth mutation that caused the Cit+ bacteria to recover and become predominant. Anyway, it appears that only two mutations were required to produce Cit+ E. coli, and those two mutations occurred at around 20,000 and 31,500 generations.

That is what the paper seems to conclude, and that makes 3 mutations.

“Seems” to conclude? Am I supposed to read minds?

Likewise, I never said it was macroevolution, just that it was “not just microevolution.”

If it’s not macroevolution, then what is the big deal about the experiment? And it could be considered microevolution — it depends on how “microevolution” and “species” are defined. To me, it’s just microevolution — the change was not that big.

It actually demonstrates your inability to read my post, as you missed the fact I never called it macroevolution.

I never said that you called it macroevolution.

And again, I can claim that a bacterium is almost ready to evolve sexual reproduction. After all, it already has mitosis working successfully and the machinery for chromosome duplication and division is already there, all it needs is to develop meiosis.

You show that you don’t understand what meiosis is — it requires the chromosomes to split into two groups, then recombine. All that was required in this experiment was just changes in single genes.

“No, I called them unimportant only for the sake of argument (“assuming arguendo,” as lawyers say). To me, they are important.”
Your capacity to retract and deny your past statements never fails to amaze me.

That wasn’t a retraction — that was a clarification! And there is nothing wrong with making a retraction if one feels that one has made a mistake.

“Here is a direct quote of Zachary, from comment #115:”
. . . .you have not provided a single quote, anywhere, where it is made clear the Cit+ was seen, in advance, as a desirable outcome.

WHAAAAAT? I just provided such a single quote — my quote from comment #115.

It would seem that, by using this experimental set-up, the original experimenters thought it was a valid approximation of nature.

There is no reason for making such an assumption. Researchers often set up laboratory experiments for what cannot be observed in nature.

After all, if it were not a valid approximation, they would not be able to draw conclusions on the real world based on the experiment.

Wrong — even if the experiment is not a valid approximation of what could occur in nature, the researchers could conclude, for example, that an unlikely occurrence in the experiment would be even more unlikely in nature.

“I said that it appears that the purpose of the glucose-cycling was to promote the evolution of Cit+ bacteria. Zachary has neither confirmed nor denied that this was the purpose of the glucose-cycling.”
Yes, and I and most others have been arguing why it wouldn’t matter either way for the experiment.

You and others have been “arguing” that point but you have not been “persuading.” So what if I don’t really “need” an answer — “O, reason not the need!” (King Lear)

Bravo on your reading comprehension.

What “reading comprehension”? You were only quoting your reply (in comment #209) to one of my statements.

Again, where has someone stated that the purpose of the pressure was to evolve Cit+ bacteria.

I am trying to find out whether that was the original purpose –or one of the original purposes — of the “pressure” of glucose-cycling. I originally assumed that it was the original purpose or one of the original purposes. I have said these things many times — you make me keep repeating myself unnecessarily.

The same pressure led to faster reproduction and higher mutation rates (though not the latter for the Cit+ strain).

How did this pressure of glucose-cycling lead to faster reproduction and higher mutation rates for the bacteria that could only eat glucose? And the glucose-cycling did potentially lead to higher mutation rates for the Cit+ strain in comparison to the strains that could only eat glucose, because the Cit+ strain could keep reproducing after the glucose supply was exhausted.

Likewise, as others have said, the same pressure could have lead to bacteria that digest other bacteria.

A much less likely outcome. As Behe said, the bacteria were close to having the ability to digest citrate.

Nowhere have you shown that the purpose was Cit+.

I am saying that this is a likely purpose and the most obvious purpose of the glucose cycling. I am trying to find out if this was an actual purpose. Duh.

I fail to see how divergence is a pompous, bombastic or ostentatious term

It is pompous, bombastic, and ostentatious only when it is claimed that it does not refer to evolution when used in this context.

Even if Cit+ had been a goal, if divergence was the overall goal, then Cit- would also have been a goal.

How could Cit- have been a goal? The bacteria were Cit- to begin with.

So your defense is to invoke invisible other readers who agree with you but refuse to post? A bold defensive strategy, to say the least.

Maybe they just think I am doing a good job of refuting you and that their help is not needed. There are a lot of “lurkers” who don’t normally get involved in discussions — that’s why they are called “lurkers.”

“I provided the quotes in comment #150″
But as I pointed out, that quote does not say that Cit+ was considered a desirable outcome

Good grief — the quote said that Cit+ evolution was foreseen as a possible outcome and it is obviously a very desirable outcome!

In post 201, when I said, “[The paper] seemed to confirm that Cit+ was not the goal for the experiment,” you responded by asking, “What other goals of the experiment does the paper mention?” While I may have paraphrased the discussion, vaguely pointing me towards the paper to refute my argument is exactly what you accuse Zachary of having done.

Wrong. Zachary answered my questions by pointing me towards the paper. In contrast, when I pointed you towards the paper I was not answering a question but was asking you a question, the question being whether the paper mentioned any goals of the experiment other than Cit+ evolution.

Previously, you said that the glucose cycling allowed silent mutations, now you claim that it reduces silent mutation?

Of course the glucose cycling tends to reduce silent mutation after the glucose supply has been exhausted, because the bacteria that can only eat glucose can then no longer reproduce, and mutations are likely to occur during reproduction. But the glucose cycling gives an advantage to the Cit+ bacteria after the glucose supply has been exhausted because they can continue reproducing, unlike their neighbors who can eat only glucose. As I said, you are making this much too complicated. Your comments here are only confusing people.

AC:

I strenuously disagree. Anything foreseen as a possible and desirable outcome is a “goal.”
According to standard definitions and usage of English words, you are, quite simply, incorrect.

I just made a long explanation as to why I am correct. You have explained nothing.

A goal can be an easy goal or a quixotic goal and anything in-between. Finding the Fountain of Youth, the Holy Grail, El Dorado, the Lost Dutchman Mine, Noah’s Ark, and the ivory-billed woodpecker have all been goals.

This, however, is simply a shame. . . . You would create a nation of overspecialized ignoramuses in the place of flexible, responsible, informed citizens.

The real shame is that when a layperson like myself educates himself and tries to enter a scientific discussion, he gets a lot of runarounds and insults.

It is pretty clear that I am wasting my time here.

rrt
June 19, 2008

Not just your time, Larry…

Kieran Lerch
June 20, 2008

I think part of the reason this has been an exercise in frustration is that it’s unclear precisely what is being argued about. Larry comes in asserting that he is asking a simple question out of idle curiosity, using the Lear quote as a characterization. But Larry, your position as a contrarian is being broadcast loud and clear throughout, whether it’s the hyperlink to your blog in every post you make or the statement that you’re a holocaust revisionist. As a consequence, people are attempting to address what they think are your concerns, and you’re goading them by dropping hints about your particular biases (eg decrying “hardline Darwin roaders”).

Larry, I know you think the burden of improvement lies with everyone else in this thread, and it might seem to be “giving in” to change your own behavior in response, but if you honestly want a higher level of discourse, or answers to your questions, here are some things I think you should try:

1. Stop insulting people. I know that you didn’t start it, and those who did made a mistake. If someone is making jabs at you it may or may not be justified to respond in kind (I personally believe it isn’t), but you’ll get more respect if you maintain a civil discourse, even from those who insulted you.

2. Try to anticipate the environment a little better. There’s a few things to consider here. One is that you might’ve tried asking one question and cutting down on the wordiness a little bit; you refined your questions as the discussion went on but it diverged into multiple lines of discourse and got pretty muddled.

The second part of this is that you might want to avoid affiliating yourself with Behe and dredging up old fights. None of the references to Behe or even your own blog were necessary for the first post you made. I know you think that this is irrational, and that you shouldn’t have to mask your perspective to get answers, but this is the reality of the argument. People will see Behe’s name, or skim your blog subject lines, or instantly assume the old fighting stance. If you really, honestly want answers to your questions, you’ll do this. If not, you’re a warrior for a different cause and your questioning really has been dishonest.

To summarize, you can’t change the environment or the people in this particular discourse, but you can change yourself or alter your approach. Find a way to do that without compromising your ability to get the answers you want and you’ll be much more satisfied.

Larry Fafarman
June 20, 2008

rrt:

Not just your time, Larry

At least you trolls got a chance to learn something — I didn’t get that chance.

Hoovooloo
June 20, 2008

“It’s not a direct answer to very simple questions, bozo!”

Again with the insults. Still, as I have said, the question may not have a simple, direct answer. Your continued refusal to read the paper is, again, why people consider you unwilling to learn.

“???? What were you going to say?”

Sorry about that. What I meant to say was that, though the mutation occurred in only 1 out of 12 populations, it occurred in 20 years. As evolution has billions of years to work in, that would hardly seem to be a big evolutionary problem (oh, and in the wild, a population that evolved a more successful trait would outcompete the other population, quickly spreading, thus 1/12 is meaningless).

“It was one little statement in eight pages of fine print and it didn’t even answer my question!”

It was not fine print. It was normal sized print. Fine print would be what was used in the footnotes and bibliography. It did, however, respond to your apparent disbelief of a third mutation. The next quote I provide from the paper should answer the “where.”

“But what caused the Cit+ bacteria to nearly disappear after growing to 19% of the population? Was that the result of a mutation? And maybe there was a fourth mutation that caused the Cit+ bacteria to recover and become predominant. Anyway, it appears that only two mutations were required to produce Cit+ E. coli, and those two mutations occurred at around 20,000 and 31,500 generations.”

Again, reading from the paper (middle of the first column, page 3), “The precipitous decline in the frequency of Cit+ cells just before the massive population expansion suggests clonal interference (47), whereby the Cit- subpopulation produced a beneficial mutant that outcompeted the emerging Cit+ subpopulation until the latter evolved some other beneficial mutation that finally ensured its persistence.” It may “appear” to you that only 2 mutations were necessary, but the paper comes to a different conclusion. Again, had you actually taken the 20 minutes to read the paper, you would know this. Oh, and the population explosion I referred to previously was the one that occurred after Cit+ nearly disappeared, so no, 3 mutations were needed at a minimum.

“”Seems” to conclude? Am I supposed to read minds?”

The quote I provided above shows that that the paper did indeed conclude what I had said. So no, you are not expected to read minds, just to have actually read the paper you claimed to have read (or rather, “browsed”).

“If it’s not macroevolution, then what is the big deal about the experiment? And it could be considered microevolution — it depends on how “microevolution” and “species” are defined. To me, it’s just microevolution — the change was not that big.”

It’s a big deal because it was a complex trait that was observed to evolve, directly refuting the arguments of many opponents of Darwinian evolution. If you consider it just microevolution, not only have you changed your mind yet again, you admit to redefining terms in science to meet your own personal beliefs. If that is the point we have reached, there is no point in debating this further, as regardless of the evidence you are provided, you can simply draw new lines to protect your precious preconceived notions.

“I never said that you called it macroevolution.”

Seeing as you spent almost all of your response to my comment trying to show that it was not macroevolution, before you finally agreed with me that it was not microevolution, you certainly seem to have been under the impression that I was claiming it was macroevolution, or else you could have simply agreed with me and saved us all a bit of reading.

“You show that you don’t understand what meiosis is — it requires the chromosomes to split into two groups, then recombine. All that was required in this experiment was just changes in single genes.”

You once again fail to have read my post. I did not claim that the bacteria was almost ready to use meiosis. Rather, I claimed that the bacteria was almost ready to evolve sexual reproduction–the mechanisms for meiosis, much as the E. coli evolved the mechanism to transport citrate across its membrane. And how would such mechanisms evolve? Through a series of changes to single genes, the same sort of changes that took place for Cit+. Unless you have some means of quantifying the difficulty of a trait to evolve, and reasons for marking some level of difficulty as “easy,” Behe’s claim remains meaningless.

“That wasn’t a retraction — that was a clarification! And there is nothing wrong with making a retraction if one feels that one has made a mistake.”

Fair enough. Of course, If you are willing to accept mistakes as a possibility, contradictions (like the one you accuse Zachary as having made) may simply be the correcting of mistakes.

“WHAAAAAT? I just provided such a single quote — my quote from comment #115.”

Again, that quote does not say that Cit+ was a goal, or that it was desirable (or more desirable than maintaining Cit-). All it states is that the citrate may present a point of divergence. Where do they say that they wanted Cit+, specifically, to evolve? Not just generally divergence, as without specifying the trait they wanted to evolve (and the citrate did lead to many traits evolving, though Cit+ was the most complex) you cannot factually state that any specific trait was a goal, by your definition of goal, or else any trait that might have evolved would be considered a goal, by the fact that it evolved.

“There is no reason for making such an assumption. Researchers often set up laboratory experiments for what cannot be observed in nature.”
–and–
“Wrong — even if the experiment is not a valid approximation of what could occur in nature, the researchers could conclude, for example, that an unlikely occurrence in the experiment would be even more unlikely in nature.”

Let me explain this to you. If the experiment had the goal of evolving Cit+, as you admit to assuming, then for the experiment to have any application, it must be about as hard, if not harder, for the bacteria to evolve Cit+ in the experiment as in the wild. If it was not, then the successful completion of the experiment (they achieved their goal) would have no meaning, as the results would tell us nothing meaningful about the likelihood in the real world. Of course, you could argue that the goal was Cit+ and they made it easier in the lab so that they could show that it was more difficult to evolve it in the wild upon the failure of the experiment. However, designing the experiment to only have an application upon failure is poor design. Unless you are also willing to state that Dr. Lenski and company cannot design an experiment, and back this claim up with evidence, the assumption that their goal was Cit+ also requires the goal of making evolution of Cit+ in the lab about as difficult as in the wild.

“You and others have been “arguing” that point but you have not been “persuading.” So what if I don’t really “need” an answer — “O, reason not the need!” (King Lear)”

Persuasion would require an open mind on your part, something that your willingness to redefine terms for your own purpose indicates you lack. If you don’t really “need” an answer, your anger at Zachary’s silence seems strange.

“What “reading comprehension”? You were only quoting your reply (in comment #209) to one of my statements.”

Yes, because in that reply I explain how the paper contradicts Behe. Your failure to understand that is the reading comprehension I referred to. I apologize for assuming you could make that connection on your own. To make it very clear, I will paraphrase the points here. Behe claims that requiring two mutations, is a big evolutionary problem, especially if one is silent. I have shown you, in the paper, where they say that at least three mutations were necessary, at least one silent, all of which occurred in less than 20 years. Thus, it would seem that having two mutations, one silent, is not as big a problem as Behe claims.

“I am trying to find out whether that was the original purpose –or one of the original purposes — of the “pressure” of glucose-cycling. I originally assumed that it was the original purpose or one of the original purposes. I have said these things many times — you make me keep repeating myself unnecessarily.”

No, you continue to insist that Dr. Lenski and Zachary have said that Cit+ was a goal (and thus a purpose) of the experiment, not try to find out if it actually was one. After all, Zachary answered you with a “no.” We have repeatedly tried to explain that they did not say Cit+ was a goal, which you seem to ignore. And on the subject of repetition, you have made me repeat why the paper contradicts Behe at least three times.

“How did this pressure of glucose-cycling lead to faster reproduction and higher mutation rates for the bacteria that could only eat glucose? And the glucose-cycling did potentially lead to higher mutation rates for the Cit+ strain in comparison to the strains that could only eat glucose, because the Cit+ strain could keep reproducing after the glucose supply was exhausted.”

I cannot answer that, as I am not a biologist. However, had you read the paper, you would see that these were indeed traits that evolved. And again, had you read the paper, you would have realized that they tested the Cit+ for increased mutation rates (hypermutability was the term they used) and found that it mutated at normal rates. Oh, and time spent reproducing!= rate of mutation.

“A much less likely outcome. As Behe said, the bacteria were close to having the ability to digest citrate.”

See my above comments on Behe. Also, Cit+ itself would seem an unlikely outcome (as you said previously, it occurred in 1 out of 12 strains). Thus, if we are ranking potential goals by the likelihood of the result to occur, Cit+ would be pretty far down on the list.

“I am saying that this is a likely purpose and the most obvious purpose of the glucose cycling. I am trying to find out if this was an actual purpose. Duh.”

And we have given you several reasons why Cit+ is NOT the most obvious and likely purpose of glucose cycling. That you continue to insist it is the most obvious and likely purpose without evidence is why you appear to be a fool. Duh.

“It [divergence] is pompous, bombastic, and ostentatious only when it is claimed that it does not refer to evolution when used in this context.”

Yet again, you fail to realize that divergence does not mean evolution, though you seem to believe the two can be used synonymously, when you claimed “”Divergence” is just a high-falutin term for “evolution”” (post 210). Divergence, in terms of evolution, is defined as “The evolution of increasing difference between lineages in one or more characters” by evolution.unibe.ch. Thus, divergence is not a “high-falutin'” term for evolution. Is a different, but related, term. Had you understood the rest of my comment, you would realize that I did use divergence in relation to evolution, in the way it is defined. Again, you are changing the definition of terms to support your own beliefs.

“How could Cit- have been a goal? The bacteria were Cit- to begin with.”

I again apologize for believing you would have been capable of making the logical leap that the goal would have been maintaining Cit-. However, my point still stands. Using the quotes you have provided, the goal would appear to be divergence, differences in evolution. If the wanted both divergence, and Cit+, they would have wanted to maintain Cit- as well, or else they would have convergence. If they want both Cit+ and to maintain Cit-, the experiment would have to be set up to favor neither, and thus the purpose of the experiment would not be Cit+.

“Maybe they just think I am doing a good job of refuting you and that their help is not needed. There are a lot of “lurkers” who don’t normally get involved in discussions — that’s why they are called “lurkers.””

If you are doing such a good job against me, you might think that one of the previous posters might have changed their minds about and posted as such. After all, they would have posted before. The one admitted lurker who as posted thus far disagrees with you. However, if you need to believe in an invisible army of supporters, good luck maintaining your sanity. Oh, and I should point out that any posts from ex-lurkers supporting you will now be suspicious. After all, it is a short hop from claiming the existence of unseen supporters to posting as them.

“Good grief — the quote said that Cit+ evolution was foreseen as a possible outcome and it is obviously a very desirable outcome!”

You keep saying it was a desirable outcome. However, you seem to be the only person that thinks that way, and you have provided no evidence to support your claim. Until you do so, you claim has no merit, and Cit+ fails to meet your own definition of a goal.

“Wrong. Zachary answered my questions by pointing me towards the paper. In contrast, when I pointed you towards the paper I was not answering a question but was asking you a question, the question being whether the paper mentioned any goals of the experiment other than Cit+ evolution.”

It also never said Cit+ was a goal, further indicating that you did not actually read the paper. Here we go: “The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue.” The goal, then, was to test historical contingency. These are the FIRST TWO SENTENCES of the paper. Just admit it: you did not read the paper, and merely claimed to have done so so people would stop calling you out on that issue. Either that, or your “deep enough” browsing involves skipping the introduction and most of the rest of the paper. Still, then, provide me with where, in the paper, it states that Cit+ was a starting goal of the experiment (not that after it happened, they realized they could use it, but that they desired it in advance).

“Of course the glucose cycling tends to reduce silent mutation after the glucose supply has been exhausted, because the bacteria that can only eat glucose can then no longer reproduce, and mutations are likely to occur during reproduction. But the glucose cycling gives an advantage to the Cit+ bacteria after the glucose supply has been exhausted because they can continue reproducing, unlike their neighbors who can eat only glucose. As I said, you are making this much too complicated. Your comments here are only confusing people.”

Sigh. Yet again you try to invoke visible mutations in this discussion. Your original quote “(1) it [glucose cycling] gave the same strains of bacteria repeated opportunities to have preliminary “silent” Cit+ mutations (by “silent” I mean not causing visible effects, such as the mutation that apparently occurred at around 20,000 generations).” Note you specifically say you are not talking about the visible (Cit+) mutation. You are saying that, somehow, the glucose cycling allowed silent mutations, (in the full quote, you seemed to imply it would allow more mutations than plentiful glucose). Now you have said, twice, that glucose cycling would reduce silent mutations. You have clearly contradicted yourself, and by your own standards, should lose all credibility. That invisible army of supporters should be abandoning you about now.

“The real shame is that when a layperson like myself educates himself and tries to enter a scientific discussion, he gets a lot of runarounds and insults It is pretty clear that I am wasting my time here.”

No, when a layperson enters a scientific discussion, refuses to educate themselves, makes claims based on nothing more than bias, and refuses to accept the evidence, they lose their credibility. When they then go on to insult other posters with stinging barbs only a first grader could create, they are ridiculed. Couple that with your inability to comprehend the paper and past posts, your inability to back your statements with evidence, your continued refusal to read the papers that are supposed to answer your questions, and your redefining of terms to make any attempt to actually have a real, evidence based, scientific discussion with you impossible, and I have given up any hope of trying to help you understand. You have not convinced me, nor do you appear to have convinced any other poster here. From this point on, if I respond at all, it will be for my own amusement and to protect others from reading your propaganda and baseless arguments unopposed.

Hoovooloo
June 20, 2008

To Kieran Lerch,
You make some excellent points, and perhaps I should tone down my posts a bit. However, you seem to assume that Larry is simply seeking responses to his question(s), and is invoking Behe out of poor decision making. His questions have been answered, by Zachary and others. He keeps finding small reasons to doubt each answer (such as the bizarre contradictions he accuses Zachary of having made without any evidence). In light of this, his purpose seems to be to repeat his same points in hope of convincing others he is right, not to actually get a response to his questions (since he did get answers).

Larry Fafarman
June 20, 2008

Kieran Lerch:

I think part of the reason this has been an exercise in frustration is that it’s unclear precisely what is being argued about.

My statements are very precise.

But Larry, your position as a contrarian is being broadcast loud and clear throughout, whether it’s the hyperlink to your blog in every post

That’s what the hyperlink is for. I use a hyperlink to highlight my name, not just to link to my blog. And many other commenters in this thread have hyperlinked their names, so why are you singling me out for criticism.

or the statement that you’re a holocaust revisionist.

I am not the one who introduced the holocaust issue here.

As a consequence, people are attempting to address what they think are your concerns, and you’re goading them by dropping hints about your particular biases

So they are not biased? Anyway, my alleged bias should have nothing to do with giving straight consistent answers to my quesitons.

Larry, I know you think the burden of improvement lies with everyone else in this thread,

I don’t just think it — I know it.

1. Stop insulting people. I know that you didn’t start it, and those who did made a mistake.

Those who insult me may expect a response in kind.

One is that you might’ve tried asking one question and cutting down on the wordiness a little bit

I asked few questions and there was no wordiness.

The second part of this is that you might want to avoid affiliating yourself with Behe and dredging up old fights.

There is nothing wrong with expressing opinions of Behe’s views.

None of the references to Behe or even your own blog were necessary for the first post you made

There is nothing wrong with on-topic links to one’s own blog. In this case, I linked to the article on my blog because that article has links to other websites. I am limited here to just one link per comment.

You have some very strange ideas about Internet etiquette.

People will see Behe’s name, or skim your blog subject lines, or instantly assume the old fighting stance.

That’s their problem, not mine.

Zachary initially caused the problem here by making confusing statements about the purposes of the experiment.

reuben
June 20, 2008

Zachary initially caused the problem here by making confusing statements about the purposes of the experiment.

Maybe so Larry, but are you now clear on the purposes? Exactly what are you confused about? You wanted to know if Cit+ was a goal of the experiment – it seems that the answer is a resounding “no”.

Is there anything else you wanted to know?

David Marjanović
June 20, 2008

Zachary initially caused the problem here by making confusing statements about the purposes of the experiment.

No, he didn’t. You just didn’t manage to read for understanding, because you had preconceived opinions about the issue that happen to be wrong.

Haven’t you noticed that the creationontheweb “article” you cite has completely misunderstood the whole experiment, for example?

You are the one who’s having a problem here. Just you. Really, go read the paper. If you can’t get it for free, ask the authors for a pdf or go to your local university library.

Larry Fafarman
June 20, 2008

Hoovooloo:

Your comments are simply getting too long for me to respond to all of your points — I will just respond to a few of them.

It was not fine print. It was normal sized print.

There is an unusually high amount of text per page — that’s why I called it fine print. And it is eight pages long.

You have a double-standard — you expect me to give direct answers to your questions or refer you to specific places that I am referring to (e.g., a comment number in this thread), yet you think it is OK to just refer me to a long paper in answering my simple, specific questions.

Again, reading from the paper (middle of the first column, page 3),

Now that’s more like it! That’s the kind of answer I am requesting. Was that so hard?

It’s a big deal because it was a complex trait that was observed to evolve, directly refuting the arguments of many opponents of Darwinian evolution.

How is it a complex trait? Michael Behe said it is a simple trait, just the ability to transport the citrate across the cell membrane:

In his new paper Lenski reports that, after 30,000 generations, one of his lines of cells has developed the ability to utilize citrate as a food source in the presence of oxygen. (E. coli in the wild can’t do that.) Now, wild E. coli already has a number of enzymes that normally use citrate and can digest it (it’s not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a “citrate permease” which can transport citrate from outside the cell through the cell’s membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, “The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.”

Hoovooloo said,

Again, that quote does not say that Cit+ was a goal, or that it was desirable (or more desirable than maintaining Cit-).

Here again, for the umpteenth time, is the quote from comment #115:

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding – I will need to check with him to make certain I understand this properly).

You folks are really hung up on this word “goal.” As I said, anything foreseen as a possible and desirable outcome is a “goal.” Finding the Fountain of Youth, the Holy Grail, the Lost Dutchman Mine, etc. have all been “goals.” You people just don’t understand the meaning of the word “goal.” OK, please, let’s forget about the word “goal” and just consider whether C+ evolution was a hoped-for result, or a wished-for result, or a longed-for result, or a prayed-for result, or wishful thinking, or whatever. And you have been ballyhooing that the Cit+ evolution — at least the “historical contingency” part — is the greatest thing since sliced bread and now you are questioning whether that evolution is “desirable.”

The goal, then, was to test historical contingency.

I presume that trying to test historical contingency was the purpose of periodically freezing samples of the populations and I therefore believe that trying to test historical contingency was an original goal of the experiment. But as I showed above, Zachary stated that he believed — subject to confirmation by Lenski — that Cit+ evolution was also an original goal of the experiment. Maybe Cit+ evolution by means of historical contingency was one of the possibilities that Lenski had in mind when he (according to Zachary) “figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit”– I don’t know. And another one of my unanswered questions is whether the purpose or one of the purposes of the glucose cycling was to try to promote Cit+ evolution. People who can’t give straight consistent answers to simple specific questions have no credibility.

You are saying that, somehow, the glucose cycling allowed silent mutations . . .Now you have said, twice, that glucose cycling would reduce silent mutations. You have clearly contradicted yourself, and by your own standards, should lose all credibility.

Yes, it is true that the glucose cycling tends to allow the silent mutations that occur during reproduction, because the bacteria that can eat only glucose can reproduce before the glucose supply is exhausted, and errors in gene duplication during reproduction are a major cause of mutations. And it is also true that the glucose cycling tends to reduce silent mutations, because the bacteria that can eat only glucose cannot reproduce after the glucose is exhausted. The extent to which the glucose cycling allows or reduces silent mutations in the glucose-eating-only bacteria depends on the ratio of the glucose feeding time to the glucose starvation time. So I have not contradicted myself.

From this point on, if I respond at all, it will be for my own amusement and to protect others from reading your propaganda and baseless arguments unopposed.

“For your own amusement”? You’re the joke.

You are just practicing oneupmanship while I am trying to find answers.

spodbox
June 20, 2008

Neat experiment. It seems to show that “micro”evolution really happens. I suspect that some mutations in the ribose permease (or other similar enzymes) gene turned it into citrate permease.

What I want to know is, how does this scale? It seemed to take 2-3 mutations to get cit+ ecoli, how many does it take to get a more complex organism a more signifcant improvement? And are those improvements even possible, given the number of “neutral” mutations (with no “bad” ones) required? This experiment can’t answer those questions.

As far as religion goes, I think that priests should stop pretending to be scientists and scientists should stop pretending to be priests. Or, as one religious paleontologist put it, “Why can’t evolution be the way God set it up to work?”

muawiyah
June 20, 2008

How did they control for possible contamination through the importation of glucose into the flasks?

Did they heat the solution to boiling first (one technique) and also make sure no thermophiles were lurking in the source material?

Seems to me you have to have to prevent the entry of any outside source of DNA not just other bacteria that may have an already expressed feature that can be “borrowed”.

Else, that foreign DNA is going to have its way with the e.coli and “fix” its problems!

Larry Fafarman
June 20, 2008

Reuben said,

Maybe so Larry, but are you now clear on the purposes? Exactly what are you confused about? You wanted to know if Cit+ was a goal of the experiment — it seems that the answer is a resounding “no”.

Both yes and no answers to that question have been given here. And just a simple “no” answer is not acceptable because it is not logical — it requires some explanation. I can think of no purpose for the glucose cycling other than to try to promote Cit+ evolution.

And you people still don’t understand the meaning of the word “goal” even after I explained it. So please, let’s forget the word “goal” and instead consider whether C+ evolution was hoped-for, or wished-for, or whatever.

David Marjanović said,

Haven’t you noticed that the creationontheweb “article” you cite has completely misunderstood the whole experiment, for example?

I don’t know — I read that article a long time ago and can’t find it now. The article looked OK as I remember it.

W. Kevin Vicklund
June 20, 2008

I strenuously disagree. Anything foreseen as a possible and desirable outcome is a “goal.”

You’re missing a vital requirement. There also has to be the intent to achieve that outcome.

A goal does not have to be a sure outcome. In fact, the word “goal” implies uncertainty.

Nice strawman. No one has argued that a goal has to be a sure outcome. That is something that you introduced on your own.

One of my printed dictionary’s definitions of “goal” is “an object or end that one strives to attain.” Note the word “strives,” which only means that there is an effort towards the goal, not that there is certainty that the goal will be attained.

You missed highlighting some vital words in that definition: “strives to attain.” Yet you explicitly acknowledge that the effort has to be made towards the goal.

The word “strives” means making an effort, and merely conducting the experiment was an effort even if nothing specific was done to try to promote the evolution of Cit+ E. coli.

And here you contradict the previous sentence. The previous sentence you state that the effort must be towards the goal, but here you claim that the effort doesn’t need to be towards the goal.

The clear meaning of the definition, and the common meaning used by nearly everybody, is that a goal requires an effort directed at producing the outcome in question. This is also the meaning explicitly used by Zachary. His answers were entirely consistent with this meaning, the usual meaning of the word. The disagreement arises because you are defining “goal” differently than he (and most of the Eglish-speaking population) does. It is your hang-up on the word “goal” that is causing all the problems, a matter of semantics on your end.

So to restate the issue of the evolution of Cit+:

1) Was it forseen as a possible outcome?

Yes.

2) Was it forseen as a desirable outcome?

Yes. (Sorry hoovooloo, but that is pretty clear)

3) Was it an intended outcome?

No.

Two out of three ain’t bad, but by the common use of the word, it’s not a goal.

4) So how did it effect the design of the initial experiment?

It didn’t. It was seen as a possible and desirable outcome of the chosen set-up, but did not play a role in the way the experiment was designed. In other words, it was not an “outcome that one [strove] to attain.” This is entirely consistent with Zachary’s comments, as well as numerous papers on the site.

Tulse
June 20, 2008

You are still playing word games. If this experiment had no goal and no purpose, then what in hell did this experiment have?

You completely missed my point. Regardless of whether the experimenters has this “goal” in mind or not (and several folks have indicated they didn’t), how would that change things for the bacteria? You don’t seem to be disputing the procedures used, merely the motivation. As far as I know, bacteria generally can’t read human intentions. So how would the goals of the experimenters impact on the results?

David Marjanović
June 20, 2008

yet you think it is OK to just refer me to a long paper in answering my simple, specific questions.

Yes, it is in fact OK. That’s how people cite scientific articles: by citing the article. You are really expected to just read it. That’s what professional scientists spend a large part of each day on.

How is it a complex trait? Michael Behe said it is a simple trait,

Please define “simple” and “complex”. If you can’t (and that’s what I expect), tell us that.

just the ability to transport the citrate across the cell membrane:

“Just”? That requires a transporter protein. Why do you think that must be easy to evolve?

and now you are questioning whether that evolution is “desirable.”

It was not expected to happen. It was a surprise. Don’t you remember? At first they thought it was a contamination.

Evidently, Zachary misremembered. As you quote, he wasn’t sure he had remembered it right; that’s why he added “(this is my understanding – I will need to check with him to make certain I understand this properly)”.

And another one of my unanswered questions is whether the purpose or one of the purposes of the glucose cycling was to try to promote Cit+ evolution.

No. The purpose was for glucose to be the limiting factor, so that higher efficiency of glucose metabolism would be selected for. (And this worked: as it turns out, it was, in fact, selected for. It just so happens that a few other things, most notably and unexpectedly citrate uptake, also evolved.)

And it is also true that the glucose cycling tends to reduce silent mutations

Wrong! It makes certain mutations silent ( = neutral = without direct or indirect effect on reproduction), others beneficial, and others harmful. In which of these categories a mutation falls depends entirely on the environment.

I can think of no purpose for the glucose cycling other than to try to promote Cit+ evolution.

Then think harder. Don’t believe that nobody else can think of something just because you haven’t thought of it so far.

I read that article a long time ago and can’t find it now.

You linked to it in comment 155 and quoted it.

—————-

What I want to know is, how does this scale? It seemed to take 2-3 mutations to get cit+ ecoli, how many does it take to get a more complex organism a more signifcant improvement?

So what if it takes a couple of million years? Where’s the problem?

And are those improvements even possible, given the number of “neutral” mutations (with no “bad” ones) required?

Why shouldn’t they be?

As far as religion goes, I think that priests should stop pretending to be scientists and scientists should stop pretending to be priests. Or, as one religious paleontologist put it, “Why can’t evolution be the way God set it up to work?”

Of course it can be. The problem is that if this idea is wrong, we cannot find that out. It is completely worthless. It can’t help us.

Then comes the principle of parsimony. If evolution can work on its own, and if evolution can also work by being a series of miracles, the first hypothesis is to be preferred, because it requires fewer ad hoc assumptions.

David Marjanović
June 20, 2008

I think Larry’s point, which he has failed to explain, is that if the evolution of cit+ was “a goal”, then Lenski et al. could have somehow set up the experiment in some biased way so that evolving cit+ would become unnaturally easy.

Is that right, and if so, how could they have done that? I can’t think of anything here… help me out, please.

Zachary
June 20, 2008

muawiyah,

When we prep DM25, we make it in four parts. The first is a salt solution, with the others being stock solutions of glucose, magnesium sulfate, and vitamin B12. All are sterilized prior to use by autoclaving, save for the B12, which is filter-sterilized. As in all microbiology work, we do all manipulations of all populations using standard aseptic technique. All the LTEE populations are regularly checked for contamination. As detailed in the paper, the Cit+ variant that evolved was verified to be descended from the founding clone of the experiment, and not a contaminant.

I am preparing a large post for Carl that is taking a little longer than I had expected (partly because I had to drive ~700 miles yesterday to come to St. Paul, MN for the Evolution conference). I apologize for the delay on that, but it should be done in the next few days (I hope). I hope that people remain interested enough to read it.

hoovooloo,

You are correct about there being evidence for at least three mutations being necessary for Cit+. There is the potentiating mutation (or mutations – we have no idea right now of knowing if there aren’t actually multiple mutations responsible for potentiation, but a single mutation is more likely), and then there are two that seem needed from there. The evidence from this is taken from the third contingency experiment. That was the one in which I plated 40 trillion (US sense) cells of clones taken from various points in the population’s history. In the 8 independent replicates among the 2800 plated, in most instances we observed that multiple Cit+ colonies grew, but did so only after long periods of incubation. This pattern, called a delayed jackpot, indicated that two mutations were required, with one occurring in the broth medium before plating (this would mean that multiple cells put on the plates had the first two mutations needed before going on the plate), and the second occurring after plating (this would explain the delay – there had to be time for the third mutation to occur before the cells started started to grow and produce colonies).

That said, what you say about the mutations that occurred after the initial evolution of Cit+ some time prior to 31,500 generations is important. It is obvious that mutations that improved Cit+ took place before the population expansion after 33,000 generations, as Cit+ clones from 33,000 generations are heritably and significantly better at growing on citrate that earlier variants. Indeed, based on what I have seen with those earlier Cit+, I am fairly sure there are likely at least 4, and maybe as many as 7 mutations that occurred during that time, with each improving performance on citrate in DM25. This is something we will be studying in work to try to sort out exactly what occurred during that period between the evolution of Cit+ and its rise to dominate population Ara-3 (but not sweep, as the Cit- cells still exist in the population even ten thousand generations later).

One last thing. I had been hoping to save this for the big post, but it is pertinent here as well. There are approximately 10^20 E. coli on Earth. That is 100,000,000,000,000,000,000 cells. That means that virtually every possible double mutation for E. coli should occur in an E. coli cell somewhere every day. Cit+ mutants likely occur pretty frequently in the total E. coli population of the planet. So how come we don’t see Cit+ E. coli that evolved it spontaneously (as opposed to getting the trait by a plasmid)? The obvious hypothesis that seems most likely is that there isn’t an empty niche into which Cit+ E. coli could move. What is more, E. coli have been around for millions of years. The LTEE has been very long and involved a great many cells for an experiment, but has been even less than pitifully small and short compared to the 4 billion year old living world.

That is just one species. There are estimated to be 10^30 total prokaryotic (those two domains of life without nuclei, made up of the Bacteria and Archaea, and composing more than half of planetary biomass) cells on Earth at any given time (I have a source on this that will be in the big post so that you can see where this number comes from). That is 1,000,000,000,000,000,000,000,000,000,000 cells. That means enormous genetic variation is being generated each day, and that is just considering mutations, and not the variation due to plasmids, horizontal gene transfer, viruses, and various recombination events. And again, this has been going on for billions of years. I don’t think many who insist that evolution is so limited even vaguely comprehend the awesome grandeur and magnitude of the living world.

Thank you,
Zachary

PS On a side note, most of the LTEE populations will have crossed the 46,000 generation mark today!

Larry Fafarman
June 20, 2008

Sheeesh — now pettifogger Kevin Vicklund (comment #231) has joined the discussion. I thought things couldn’t get worse, but they did.

Kevin, you are just playing word games. If Cit+ evolution was foreseen as a possible and desirable outcome of the experiment, then Cit+ evolution was a goal of the experiment. The effort of conducting the experiment was an act of “striving” towards that goal even if nothing specific was done to try to promote Cit+ evolution (I think that the purpose or one of the purposes of the glucose cycling was to try to promote Cit+ evolution). But since you folks cannot understand a simple, everyday word like “goal” even after the meaning is carefully explained to you, I asked that we just forget about the word “goal” and concern ourselves with whether Cit+ evolution was hoped-for or wished-for or whatever.

David Marjanović said (comment #233) —

yet you think it is OK to just refer me to a long paper in answering my simple, specific questions.
Yes, it is in fact OK.

It is sometimes OK. It was not OK here.

You folks have a double standard. You expect me to give direct answers to your questions but think that bibliography-bluffing is OK in responding to my questions.

“Just”? That requires a transporter protein. Why do you think that must be easy to evolve?

It is comparatively easy to evolve.

and now you are questioning whether that evolution is “desirable.”

It was not expected to happen. It was a surprise.

But if it was foreseen as a possible and desirable event, then it was a goal. If it was a goal but a long-shot goal, then it should be called a long-shot goal. Anyway, I proposed that we stop using the word “goal” here because you folks don’t understand the word’s meaning.

No. The purpose was for glucose to be the limiting factor, so that higher efficiency of glucose metabolism would be selected for.

Selection for higher efficiency of glucose metabolism would occur without limiting the glucose supply. I assert that it appears that the purpose or one of the purposes of giving an insufficient supply of glucose was to try to promote evolution of citrate-eating bacteria.

And it is also true that the glucose cycling tends to reduce silent mutations
Wrong! It makes certain mutations silent

How many times do I have to repeat myself? I said that the glucose cycling tends to reduce silent mutations because the bacteria that can eat only glucose cannot reproduce after the glucose supply is exhausted, and errors in gene duplication during reproduction are a major source of mutations. Suppose, for example, instead of starting new populations every day, the populations were kept for a year and were still given just a few hours of glucose supply. That would make it quite obvious that the glucose cycling tends to reduce silent mutations in the bacteria that can eat only glucose.

You linked to it in comment 155 and quoted it.

So how does the article misinterpret the experiment? And please don’t accuse me of bibliography-bluffing just because I am referring you to the entire article — I am asking a question, not giving an answer.

The rest of your comment (#233) is a response to another commenter. You ought to identify who you are responding to so that people won’t think that you are responding to me (especially when your comment starts with responses to me). It is especiall annoying that some people may think that I made statements that another commenter made.

David Marjanović said in another comment (# 234) —

I think Larry’s point, which he has failed to explain, is that if the evolution of cit+ was “a goal”, then Lenski et al. could have somehow set up the experiment in some biased way so that evolving cit+ would become unnaturally easy.

A goal does not have to be easily attainable. Finding the Fountain of Youth, the Lost Dutchman Mine, etc. have been goals but not easily attainable goals. Anyway, as I said, IMO we should stop using the term “goal” here because you folks can’t understand its meaning.

Kieran Lerch
June 20, 2008

Larry, if you weren’t so combative you might have noticed my post wasn’t a criticism of you; if anything, it was a criticism of human standards of discourse. I’m maybe the only person in these comments that has given you the benefit of the doubt. Your selective quoting (you quote the first part of my first suggestion and respond, when the second half preempts your response) and misunderstanding of almost everything I wrote suggest I was wrong to give you the benefit of the doubt.

Tulse
June 20, 2008

If Cit+ evolution was foreseen as a possible and desirable outcome of the experiment, then Cit+ evolution was a goal of the experiment. The effort of conducting the experiment was an act of “striving” towards that goal even if nothing specific was done to try to promote Cit+ evolution

Even if that were true, so frickin’ what? Unlike supernatural beings, experimenters can’t influence the physical world via a pure act of will. Unless you are either a) objecting to some specific aspect of the reported procedure, or b) accusing the experimenters of misreporting their methodology and committing scientific fraud, then you’ve got no argument.

W. Kevin Vicklund
June 20, 2008

I asked that we just forget about the word “goal” and concern ourselves with whether Cit+ evolution was hoped-for or wished-for or whatever.

Which I did. I notice that you completely ignored that portion of my post. To restate what I said:

Zachary’s comments are entirely consistent with the premise that Cit+ evolution was seen as a possible and a desirable outcome, but not an intended outcome. That means that the design of the LTEE was not driven in any way by the desire to produce a Cit+ strain.

This is what you say you wanted to discuss. So discuss it.

W. Kevin Vicklund
June 20, 2008

semantic quibble: it should be “by a desire” not “by the desire” in my previous comment.

Hoovooloo
June 20, 2008

Thank you Zachary, for your response. Oh, and I might have missed this at the end of the paper, are there any plans when the LTEE will stop in the future, or will it continue as long as there is funding?

“Your comments are simply getting too long for me to respond to all of your points — I will just respond to a few of them.”

A convenient way to dismiss/ignore my points, but I’ll go with it for now, which is why this post is

Hoovooloo
June 20, 2008

Sorry about that, cutting and pasting works strangely. I was going to say that my last post was less than half the length of my past ones.

Zachary
June 20, 2008

Hoovooloo,

>Oh, and I might have missed this at the end of the paper, are there any plans when the LTEE will stop in the future, or will it continue as long as there is funding?

Karl
June 20, 2008

Evolutionists are bluffing when they say their beliefs are scientific. Be sure to look at the list of evolutionists who refuse the debate challenge from Dr. Joseph Mastropaolo. See the list at http://www.lifescienceprize.org/.

Carl Zimmer is #146.

Hoovooloo
June 20, 2008

Oh, come on now Karl, that is no evidence. First of all, what qualifies a Judge as a scientifically literate evaluator of evidence? Secondly, how does a successful author refusing to engage an admitted creationist in some contrived publicity stunt prove that the author’s beliefs are unscientific? Finally, why do you believe a debate in person is a good way to evaluate theories? It can take long time to dig through all the evidence, to throughly evaluate it, to check that the evidence and experiments are valid. That you belief refusal to engage in a publicity stunt with someone is evidence that a belief is unscientific shows you do not understand what the term “scientific” means.

Larry Fafarman
June 20, 2008

Kevin Vicklund said(comment #239) —

Zachary’s comments are entirely consistent with the premise that Cit+ evolution was seen as a possible and a desirable outcome, but not an intended outcome

Sheeeesh — you can’t “intend” an outcome that you do not have complete control over!

That means that the design of the LTEE was not driven in any way by the desire to produce a Cit+ strain.

For the umpteenth time — I and others assumed that the purpose or one of the purposes of the glucose cycling (alternating glucose feeding and glucose starvation) was to try to promote the evolution of a Cit+ (citrate-eating) strain. For the umpteenth time — there has been no answer as to whether that was a purpose of the glucose cycling. For the umpteenth time — I have not gotten an answer to the question of whether there was any other purpose for the glucose cycling (calling the glucose cycling an “environmental stressor” is not an answer). For the umpteenth time — glucose feeding had the effect of allowing “silent” mutations during reproduction of the Cit- (eating only glucose) bacteria and glucose starvation gave an advantage to Cit+ bacteria, which could continue to reproduce after the glucose was exhausted.

Kieran Lerch said(comment #237) —

Larry, if you weren’t so combative

Of course I’m combative — because I am constantly being confronted with bullshit here. Also, Sleazy PZ Myers sent his goons here to attack me.

you quote the first part of my first suggestion and respond, when the second half preempts your response

No, the second half of your comment preempted nothing. I am not going to change my behavior to accommodate hostile commenters.

But experimenters can have goals, or “hoped-for results,” or “wished-for results,” or whatever. And the experimenters can influence the results to a limited extent — for example, the glucose cycling has the effect of tending to promote evolution of Cit+ mutants, as I discussed above.

Hoovooloo said (#241) —

I never demanded a simple, direct answer to my questions.

Oh, no, nothing like that.

The only evidence that you have provided are the quotes from Zachary

He is a co-author of the paper and you call the quotes from him the “only” evidence?

Would you extend me the same courtesy and provide me with direct quotes from the paper supporting your statements?

Why do I have to quote from the paper? Why can’t I quote from elsewhere or just make up my own ideas?

until you have some way to quantify and evaluate difficult versus easy in evolution, that statement remains meaningless.

You say that the evolution observed here is difficult, so how do you define “difficult” evolution?

According to Princeton, a goal is “the state of affairs that a plan is intended to achieve and that (when achieved) terminates behavior intended to achieve it.”

That’s absurd. Anyway, please, let’s stop using the word “goal,” because we can’t agree on its meaning.

“The extent to which the glucose cycling allows or reduces silent mutations in the glucose-eating-only bacteria depends on the ratio of the glucose feeding time to the glucose starvation time.”
What do you mean by reduces? If you mean the rate at which mutations occur, then that is only affected by mutagens in the environment/ error rates of the cellular mechanisms, both of which glucose would not effect.

Since errors in gene duplication during reproduction are a major source of mutations, preventing reproduction by glucose starvation would tend to reduce the rate at which mutations occur.

When you first posted on this subject, you were contrasting glucose cycling with plentiful glucose. Thus, the implication was that you thought glucose cycling would allow more mutations than plentiful glucose. You now deny that claim. Thus, you contradicted yourself.

I don’t care what I said when I first posted on this subject — I have since clarified my statements in case they were misunderstood. Sheeeesh.

Your arguments here are just a lot of sophistry.

Kieran Lerch
June 20, 2008

If you’re not willing to change your behavior, then you don’t really want answers more than you wish that you could have discussions in some sort of ideal environment where everyone is the perfect discussion partner. It’s a nice idea, but it’ll never happen and forging ahead like it already is that way doesn’t solve a thing. So which will it be, answers or delusion?

Hoovooloo
June 21, 2008

“He is a co-author of the paper and you call the quotes from him the “only” evidence?”

You are the one trying to convince us that he is not credible. If we assume, for a moment, that you are correct, then his quotes are not evidence that Cit+ was a “goal,” as neither quote would have been credible. If we assume you are incorrect, then there is no contradiction, and he answered you with a no.

“Why do I have to quote from the paper? Why can’t I quote from elsewhere or just make up my own ideas?”

You can, but you will still need evidence for the claims, else they lack credibility. The paper was peer-reviewed and goes through all the evidence they used to draw their conclusions. Your sources and personal ideas, however, do not.

“You say that the evolution observed here is difficult, so how do you define “difficult” evolution?”

If I ever used the term “difficult,” I apologize (and would like you to point out where). I should have used “not easy,” as in “there is no clear way to define an evolutionary event as difficult or easy”. Still, though, you have not provided any evidence, or a means to quantify difficulty, to support Behe’s quote.

“That’s absurd. Anyway, please, let’s stop using the word “goal,” because we can’t agree on its meaning.”

If it were so absurd, you might think Merriam-Webster would significantly differ in their definition (they don’t). Both define a goal as needing intent. Your own usage would require a goal to require intent. After all, if you claim a goal does not require intent, then even if Cit+ meets your definition of a goal, there is still no evidence that the experiment was set up to achieve this goal (had the “intent” of evolving Cit+).

“Since errors in gene duplication during reproduction are a major source of mutations, preventing reproduction by glucose starvation would tend to reduce the rate at which mutations occur.”

Again, you do not understand what rate means. However, you would realize that I preempted your response in my post. Using your own definition, glucose cycling would reduce the rate/number of silent mutations that would occur, thus making it more difficult to evolve Cit+ in the lab than the wild. If we use your definition, then the experiment was clearly not designed to promote Cit+ evolution, as it makes it more difficult than in the wild.

“I don’t care what I said when I first posted on this subject — I have since clarified my statements in case they were misunderstood. Sheeeesh.”

So when you contradict yourself, you are merely correcting past statements, but when Zachary contradicts himself (allegedly), there is no chance that he made a mistake previously? Sheeeesh.

But experimenters can have goals, or “hoped-for results,” or “wished-for results,” or whatever.

I repeat…so frickin’ what? Why does what they “hoped for” matter in terms of the outcomes? I can hope with all my might that when I bake a Betty Crocker chocolate cake it will turn out to be orange sherbet, but no matter how much I may hope, as long as I follow the procedures laid out my “hoped-for results” won’t change the outcome. Ditto with scientific methodology.

And the experimenters can influence the results to a limited extent — for example, the glucose cycling has the effect of tending to promote evolution of Cit+ mutants, as I discussed above.

If you want to argue that the experimental methodology promoted this particular evolutionary step, then say that, rather than talking endlessly about “goals” and “hoped-for results”. Intentions don’t matter in science — what matters is what was actually done.

And to be honest, I have no idea why you think that your overall point is somehow telling. Yes, the bacteria were subjected to an environment where it would have been beneficial for them to evolve to metabolize citrate, and a small population of them did just that. How is that not evolution, no matter what the experimental setup?

Larry Fafarman
June 21, 2008

Hoovooloo:

You are the one trying to convince us that he is not credible.

His own failure/refusal to answer my simple, basic questions here shows that he is not credible.

If I ever used the term “difficult,” I apologize (and would like you to point out where). I should have used “not easy,”

Difficult, not easy, what’s the difference? They are both still qualitative, not quantitative, terms.

If it were so absurd, you might think Merriam-Webster would significantly differ in their definition (they don’t).

Wrong. My Webster’s printed dictionary’s applicable definition of “goal” is “an object or end that one strives to attain.” Your definition, from “Princeton,” whatever that is, says a goal is “the state of affairs that a plan is intended to achieve and that (when achieved) terminates behavior intended to achieve it.” That’s absurd. “Terminates behavior”? In sports, does a game end when a goal is made? Also, “intent” should not be part of the definition because often there is incomplete control over whether the goal will be achieved. In sports, a team “tries” to score a goal — a team does not “intend” to score a goal. Anyway, I asked that we stop using the term “goal” because we cannot agree on its definition.

Again, you do not understand what rate means. However, you would realize that I preempted your response in my post. Using your own definition, glucose cycling would reduce the rate/number of silent mutations that would occur, thus making it more difficult to evolve Cit+ in the lab than the wild. If we use your definition, then the experiment was clearly not designed to promote Cit+ evolution, as it makes it more difficult than in the wild.

You still don’t get it. I will go over this one more time.

The carefully controlled daily glucose cycling in a citrate-rich medium, where the population starts growing in the morning and the glucose is exhausted by the afternoon, has the following combination of effects that tend to promote Cit+ evolution: (1) there is opportunity for silent mutations during reproduction of the Cit- bacteria during glucose feeding and (2) Cit+ mutants have an advantage during glucose starvation because they can continue reproducing while their Cit- neighbors cannot. This precise daily glucose cycling in a citrate-rich medium is not likely to occur in nature, so I assert that Cit+ evolution is more likely in this experiment than in the wild. Also, the following additional features of the experiment cannot occur in nature: (1) 12 separate lines of bacteria descended from a single individual, (2) new populations started each day, (3) protection against contamination of the lines of bacteria, and (4) continuation of the experiment for 20 years. So this experiment is quite a bit different from anything that could occur in nature.

So when you contradict yourself, you are merely correcting past statements, but when Zachary contradicts himself (allegedly), there is no chance that he made a mistake previously?

I clarify my statements when apparent contradictions are pointed out — Zachary does not.

You are completely illogical and nonsensical. Trying to debate you makes me feel like I am trying to spoonfeed an uncooperative baby who keeps knocking away the spoon and spattering the food and making a big mess.

Larry Fafarman
June 21, 2008

Tulse said (#249) —

Why does what they “hoped for” matter in terms of the outcomes?

The outcomes of experiments are influenced — though are not necessarily entirely determined — by the ways that the experiments are designed, and the ways that experiments are designed are determined by the experimenters’ hopes and expectations. That is so obvious that it should not be necessary to point it out.

And the experimenters can influence the results to a limited extent — for example, the glucose cycling has the effect of tending to promote evolution of Cit+ mutants, as I discussed above.
If you want to argue that the experimental methodology promoted this particular evolutionary step, then say that, rather than talking endlessly about “goals” and “hoped-for results”.

That is what I said, isn’t it? But I am trying to confirm that promoting this particular evolutionary step, Cit+ evolution, was in fact a purpose of this experimental methodology, glucose cycling, and I am not getting any straight answers. One commenter said that this glucose cycling is an “environmental stressor,” and that is not an acceptable answer. Zachary created confusion by saying that Cit+ evolution was not a “goal” of the experiment even though this particular experimental methodology, glucose cycling, appears to be an effort to promote that goal. And I asserted that a “goal” could be anything foreseen as a possible and desirable outcome of the experiment and that hence Cit+ evolution could have been a goal even if nothing specific was done to try to promote it, but then commenters here introduced crazy definitions of “goal” and so I asked that we not use that term but use terms like “hoped-for result” and “wished-for result” instead. And the reason why I have been “talking endlessly about ‘goals’ and ‘hoped-for results’ ” is that I have not been getting straight, consistent answers to my questions. . Zachary has not clarified his statements. This is not a matter of interpretation of the results — this is just a matter of answering some simple, basic, objective questions.

Zachary and his paper have no credibility because he won’t answer some simple, basic, objective questions about it. Zachary and his supporters have long ago passed the final point where they could redeem themselves by giving straight, consistent answers to my questions.

This paper has attracted a tremendous amount of reviews and comments. I hope that a lot of people will see this thread so that Zachary and his paper will be thoroughly discredited.

Dave Godfrey
June 21, 2008

The only goal of the experiment was to see what happens when you allow bacteria to evolve for 20 years in a particular environment. Cit+ was just one of many adaptations that the experiment allowed for. Suspended animation or cannibalism might evolve as the experiment continues, but the experiment was not set up to get any of those results deliberately.

Larry, if you had responded to the questions asked of you by citing the literature, people wouldn’t object. They’d go and read the paper/webpage/etc. One of the most common things to see on the various palaeontology mailing lists are requests for references, and links to PDFs.

Tulse
June 21, 2008

The outcomes of experiments are influenced — though are not necessarily entirely determined — by the ways that the experiments are designed, and the ways that experiments are designed are determined by the experimenters’ hopes and expectations. That is so obvious that it should not be necessary to point it out.

What should be obvious is that the pertinent issue is the experiment methodology, and not the goals or intents, since all the bacteria “see” are the procedures used, and not the experimenters’ allegedly “desired” results. All this talk of “goals” is mere distraction — if you think the methodology biased the study outcome, then deal with those specific methodological issues. Prattling on about “goals”, as if those things in themselves were relevant, is just damned silly.

I’ll put this more simply — the bacteria don’t care what the “goals” are of the experiment. Address what happened to the bacteria, and not what the experimenters did or didn’t “hope for”.

Hoovooloo
June 21, 2008

“His own failure/refusal to answer my simple, basic questions here shows that he is not credible.”

He did answer you, with a no. And you again missed my point, which was that if we assume you are correct, and he is not credible, then his quotes are not valid evidence as to what the purpose of the experiment was. Thus, we have to look at the paper, which provides us with a goal other than Cit+.

“Difficult, not easy, what’s the difference? They are both still qualitative, not quantitative, terms.”

Yet again, you missed the rest of my post. I explained that by “not easy,” I meant that you could not classify it as easy or difficult. So, now we are in agreement, and the quote you had from Behe is still meaningless.

“Wrong. My Webster’s printed dictionary’s applicable definition of “goal” is “an object or end that one strives to attain.”

So the one difference is that Princeton claims that the goal terminates the activity? Well, then, let’s drop that part and use the part of the definition where they agree. Both definitions still require intent, not just a “hoped-for” result.

“Anyway, I asked that we stop using the term “goal” because we cannot agree on its definition.”

Too bad. You are trying to claim that, since Cit+ was both possible and desirable, it was a goal (the experiment was set up to achieve it). Thus, having a “goal” implies having intent. If we redefine/replace “goal” as a “hoped-for” result, it provides no support that the experiment was designed to evolve Cit+. Think of it this way. Say we were testing a drug to prevent Alzheimer’s. Of course, the human body is a vastly complex system, so we do not know exactly what the drug will do. It may end up curing cancer, which would certainly be a desirable result. But was the intent of the experiment to find a cure for cancer? Was the experiment designed explicitly to cure cancer? No, it was designed to test a potential cure for Alzheimer’s disease, even if one of the researchers thought, “it would be awesome if this cured cancer.”

“The carefully controlled daily glucose cycling in a citrate-rich medium, where the population starts growing in the morning and the glucose is exhausted by the afternoon, has the following combination of effects that tend to promote Cit+ evolution: (1) there is opportunity for silent mutations during reproduction of the Cit- bacteria during glucose feeding and (2) Cit+ mutants have an advantage during glucose starvation because they can continue reproducing while their Cit- neighbors cannot”

Yet again, I must remind you that we are not discussing how glucose cycling effects Cit+ bacteria after they have evolved. If you would like to start a new discussion on that, fine, but stop changing the subject to avoid answering. You have claimed 2 things here: That glucose cycling allows silent mutations, and that glucose cycling reduces silent mutations. You have stated those explicitly, and claim the you actually meant the latter of the two statements. Since Cit+ requires at least one silent mutation, designing the experiment to reduce the number of silent mutations would make it more difficult to produce Cit+. Thus, if you insist that glucose cycling would reduce silent mutations, the experiment was not designed to promote Cit+. How the environment effects Cit+ bacteria following their evolution is mostly meaningless in determining if the environment was created to evolve Cit+ (it only effects the spread/growth of Cit+ AFTER it has evolved).

It took several posts after I pointed out your silent mutation contradiction before you claimed that you were simply correcting a mistake. Why should Zachary respond, again, to someone with such a hostile attitude?

“You are completely illogical and nonsensical.”

Show me where. I have shown many places where you were wrong, contradicting yourself or making baseless claims. You have not shown me one place, with quotes/post numbers, where I have contradicted myself. Likewise, the majority here seem in agreement with me.

Hoovooloo
June 21, 2008

“Zachary created confusion by saying that Cit+ evolution was not a “goal” of the experiment even though this particular experimental methodology, glucose cycling, appears to be an effort to promote that goal.”

No, you believe that glucose cycling promotes Cit+ evolution. Not only is that wrong, as I pointed out above, but one of the researchers, Zachary, told you that Cit+ was not a purpose of the experiment. A “hoped for” result does not mean that the experiment was designed to achieve said result. Again, as I pointed about above, your description of how glucose cycling effects the bacteria implies that Cit+ was not a goal.

“I hope that a lot of people will see this thread so that Zachary and his paper will be thoroughly discredited.”

And the truth is finally revealed. Self-education is not your purpose, as you claimed. Your purpose is to spam the comments with the same, disproven rhetoric in hopes of tricking people into believing you.

Larry Fafarman
June 21, 2008

Dave Godfrey said,

Cit+ was just one of many adaptations that the experiment allowed for.

I have said a zillion times that it appears that the purpose or a purpose of the glucose cycling (alternating glucose feeding and glucose starvation) was to try to promote Cit+ evolution. I never got a confirmation or denial of that.

Larry, if you had responded to the questions asked of you by citing the literature, people wouldn’t object.

Sheeesh — why do I have to cite the literature? And I did cite the literature where appropriate — Behe’s review of the article, the article linked to in comment #155, and the original post.

Tulse said,

if you think the methodology biased the study outcome, then deal with those specific methodological issues.

I did deal with methodological issues — I said that I assumed that the purpose of the glucose cycling was to try to promote Cit+ evolution. And I have also said a zillion times that Cit+ evolution could have been a goal or a hoped-for or wished-for result even if nothing specific had been done to favor Cit+ evolution.

Hoovooloo:

He did answer you, with a no.

For the zillionth time, he did not give straight and consistent answers to my questions. And he never answered my question about whether the glucose cycling was intended to favor Cit+ evolution.

now we are in agreement

No, we are not in agreement.

So the one difference is that Princeton claims that the goal terminates the activity? Well, then, let’s drop that part and use the part of the definition where they agree. Both definitions still require intent, not just a “hoped-for” result.

Where in hell did this “intent” shit come from as part of the definition of “goal”? “Intent” often implies (though not always) that there is complete control over the outcome. In sports, a team “tries” to score a goal — a team does not “intend” to score a goal. I am getting hit with this “intent” shit from both ends — you say that “intent” is everything and Tulse says that “intent” is nothing (he says that the bacteria don’t care what the intent of the researchers is). You people are just playing word games, and I am sick of it.

Since Cit+ requires at least one silent mutation, designing the experiment to reduce the number of silent mutations would make it more difficult to produce Cit+. Thus, if you insist that glucose cycling would reduce silent mutations, the experiment was not designed to promote Cit+.

The glucose starvation phase was a trade-off so far as promoting Cit+ evolution was concerned — it tended to reduce silent mutations by preventing reproduction of the Cit- bacteria but gave a reproductive advantage to the Cit+ bacteria.

It took several posts after I pointed out your silent mutation contradiction before you claimed that you were simply correcting a mistake.

There was no real contradiction and I clarified my statements immediately.

You have not shown me one place, with quotes/post numbers, where I have contradicted myself.

Even if you have not contradicted your bullshit, it is still bullshit.

Likewise, the majority here seem in agreement with me.

There has been no scientific polling of the readers here.

“I hope that a lot of people will see this thread so that Zachary and his paper will be thoroughly discredited.”
And the truth is finally revealed. Self-education is not your purpose, as you claimed.

When I started commenting here, it was not my purpose to discredit the paper.

The only reason why I am still responding to your crap here is that many of the readers automatically assume that you are right and I am wrong, so it is necessary to defend myself.

Owlmirror
June 21, 2008

When I started commenting here, it was not my purpose to discredit the paper.

Oh? So you mean that is your purpose now? It seems quite clear, given your obvious bias, that that was a “wished-for” result.

Larry Fafarman
June 21, 2008

When I started commenting here, it was not my purpose to discredit the paper.

Oh? So you mean that is your purpose now?

What do you expect when I can’t get straight consistent answers to simple, basic, objective questions?

Owlmirror
June 21, 2008

What do you expect when I can’t get straight consistent answers to simple, basic, objective questions?

But your questions were not, in fact, objective. You wanted to know what was “wished-for” or “hoped-for” — and wishing and hoping are subjective emotions.

An objective question would be about the objective results, which were indeed presented in the paper and the postings about it.

Cynthia Wood
June 21, 2008

Larry – your comment about the credibility of the paper being affected by this thread is having two effects here in this household (though I doubt either one was the goal). The first is drop-jawed incredulity. The other is gales of laughter. The research (and hence the paper) is credible or not credible based on the science in the paper. Post-publication, it doesn’t (and shouldn’t) matter WHAT the scientist does in discussions – particularly random blog discussions with random non-colleagues. Some (many) scientists aren’t particularly adept at ad-hoc discussion with people who aren’t familiar with the particulars of their field. It doesn’t have thing one to do with the soundness of their science.

Excuse me, I’m going to go get my husband and show him this one. He needs a laugh.

Larry Fafarman
June 21, 2008

Owlmirror driveled,

But your questions were not, in fact, objective. You wanted to know what was “wished-for” or “hoped-for” ? and wishing and hoping are subjective emotions.

Those are not “emotions” — but even if they were, the question is whether those emotions existed, which is an objective question.

Cynthia Wood barfed,

Post-publication, it doesn’t (and shouldn’t) matter WHAT the scientist does in discussions – particularly random blog discussions with random non-colleagues. Some (many) scientists aren’t particularly adept at ad-hoc discussion with people who aren’t familiar with the particulars of their field.

You are so full of living crap, you lousy dunghill, that it is coming out of your ears. My questions were simple and basic, e.g.,

(1) Was Cit+ evolution a goal (or a hoped-for result or a wished-for result) of the experiment?

(2) Was the purpose or one of the purposes of the glucose cycling (glucose feeding followed by glucose starvation) to try to promote Cit+ evolution? (the combination of a yes answer to this question and a no answer to the first question are inconsistent)

(3) What were other purposes of the glucose cycling, if any?

If you want to see some folks who are really making unreasonable requests for information about the experiment, then I suggest that you go over to Conservapedia, where they are asking for the raw data —

You, Zachary, Lenski, Hoovooloo, etc. can take this lousy paper and jump in the lake.

kal
June 21, 2008

Ladies and gentlemen…

Larry Fafarman!

At 62, the world’s oldest baby!

Give the infant a hand!

Larry Fafarman
June 21, 2008

Never have I seen people so unconcerned about their credibility. Once credibility is lost, it is difficult or impossible to regain.

kal
June 21, 2008

You would know…wouldn’t you, laughingstock Larry?

Cynthia Wood
June 22, 2008

Larry, you lost your credibility as a critic long, long ago on this thread.

And what happens in this thread has about as much power to discredit the MSU paper as an internet discussion on diving has to call one of Greg Louganis’s gold medals into question. I.e. None whatsoever.

The internet sure gives some people delusions of grandeur. Or possibly delusions of relevence.

Cynthia Wood
June 22, 2008

On your simple basic questions #3 – you can answer that question yourself in less than five minutes by reading the article that heads this discussion thread.

Issues like this may be why people are less than convinced of your indignation at not having your questions answered.

But do go on insulting people. I haven’t had so much fun since a Vox Day fan called me a raddled old harridan.

Hoovooloo
June 22, 2008

“I have said a zillion times that it appears that the purpose or a purpose of the glucose cycling (alternating glucose feeding and glucose starvation) was to try to promote Cit+ evolution. I never got a confirmation or denial of that.”

And for the zillionth time, yes you did. Zachary said Cit+ was not a goal of the experiment. Hence, Cit+ was not a goal of glucose starvation. That is what we call a denial. Now you are trying to argue that Zachary is lying, an entirely different issue.

“why do I have to cite the literature?”

To show that there is scientific reasoning behind your claims (necessary for your credibility).

“And I have also said a zillion times that Cit+ evolution could have been a goal or a hoped-for or wished-for result even if nothing specific had been done to favor Cit+ evolution.”

Okay, but if nothing was done to favor Cit+ evolution, the paper and results are credible. Also, how and why would Zachary answer questions about his and other’s personal emotions that, by your own admission, may have nothing to do with th experiment’s results?

“Where in hell did this “intent” shit come from as part of the definition of “goal”? “Intent” often implies (though not always) that there is complete control over the outcome.”

This is just wrong. Look at your definition of goal. The one pulled from your (Webster) dictionary. Now look up intent. Going by Princeton (my dictionary), the relevant definition is “an anticipated outcome that is intended or that guides your planned actions” Nothing in there about complete control. If a result is simply “wished for,” or a “goal” by your definition, it does not imply anything in the experiment was designed to reach that result. Thus, even if Zachary “wished for” a result, it does not mean the experiment was designed to produce that result, nor that he contradicted himself

That the newly evolved trait fits the environment well does not mean the environment was designed for that trait. After all, natural selection works to produce traits that function well in the given environment. Using your logic, it could be said that the experiment was designed specifically for any trait that ended up evolving.

“Even if you have not contradicted your bullshit, it is still bullshit.”

Not if you can’t prove it is bullshit.

“it is necessary to defend myself.”

Unless you are wrong

“http://www.conservapedia.com/Conservapedia_talk:Lenski_dialog”

Glad to see you are keeping bias out of your references.

“You, Zachary, Lenski, Hoovooloo, etc. can take this lousy paper and jump in the lake.”

This is the amusement I was talking about

Larry Fafarman
June 22, 2008

Cynthia Wood driveled,

On your simple basic questions #3 – you can answer that question yourself in less than five minutes by reading the article that heads this discussion thread.

Even if a question has already been answered, that is no reason to not answer it again or point out where it has been answered.

The only thing in the original article that addresses my question #3 is the following statement:

Lenski and his colleagues have also shown how natural selection has demanded trade-offs from the bacteria; while they grow faster on a meager diet of glucose, they’ve gotten worse at feeding on some other kinds of sugars.

Now what does that statement say? Does it say that the bacteria “grow faster on a meager diet of glucose” than they do on a full diet of glucose? That’s absurd. Or does it say that they grow faster on a meager diet of glucose than on meager diets of other kinds of sugars? The statement requires some explanation.

Also, even if there were other reasons for the glucose cycling, that is no reason for not answering the question of whether promoting Cit+ evolution was a reason for the glucose cycling.

Hoovooloo moaned,

“I have said a zillion times that it appears that the purpose or a purpose of the glucose cycling (alternating glucose feeding and glucose starvation) was to try to promote Cit+ evolution. I never got a confirmation or denial of that.”
And for the zillionth time, yes you did. Zachary said Cit+ was not a goal of the experiment. Hence, Cit+ was not a goal of glucose starvation. That is what we call a denial.

That is not a direct answer to the question! Why must I guess at answers instead of getting direct answers? And a direct answer to that question would be a quality-control check on his claim that Cit+ mutation was not a goal of the experiment! Checking the consistency of answers to different questions is a way of discovering errors in the answers or misunderstandings in interpreting the answers! For example, Zachary’s interpretation of the word “goal” might be different from my interpretation of the word — your interpretation and my interpretation of the word are certainly vastly different!

Now you are trying to argue that Zachary is lying, an entirely different issue.

If he won’t give straight answers to my questions, he is no better than a liar.

“why do I have to cite the literature?”

To show that there is scientific reasoning behind your claims (necessary for your credibility).

Why? You don’t always cite the literature to show that there is scientific reasoning behind your claims.

Okay, but if nothing was done to favor Cit+ evolution

Something was done that favored Cit+ evolution: the glucose cycling. I am trying to find out whether this was an intended purpose of the glucose cycling. If it was an intended purpose of the glucose cycling, then Zachary’s statement that Cit+ evolution was not a “goal” (or a hoped-for result or wished-for result or whatever) is obviously wrong.

Now look up intent. Going by Princeton (my dictionary), the relevant definition is “an anticipated outcome that is intended or that guides your planned actions.”

That is your dictionary’s definition of “intent” — “an anticipated outcome”? You have one screwed-up dictionary.

Anyway, you ignored my little example: a sports team scores a goal by “trying” to score a goal, not by “intending” to score a goal. “Intent” is not an appropriate part of the definition of “goal.”

Anyway, instead of forcing me to guess answers according to indirect hints and the connotations of different words, why not just give direct, unambiguous answers and clear up misunderstandings if they occur?

Larry, the experiment was performed to see what happens to E. coli when put on a starvation diet for a very long period of time. One of the easiest ways of doing this is glucose cycling. Citrate was included to test for contamination, because E. coli can’t normally use it.

Any result they have published on could be a “hoped for” one- they hoped the bacteria would adapt.

Cit+ was one way the bacteria could evolve. But it wasn’t considered particularly likely, as the investigators thought the experiment had been contaminated- which is what the citrate was there to test for.

The bacteria don’t care what the humans want to happen, they will grow and mutate at random, the experiment isn’t going to make one mutation more likely to occur than another.

Regardless of what the experimenters might have liked to see, the experiment is not nearly directed enough for them to be able to control in which way the bacteria evolve.

You’ve cited three review articles. None of them are original research. Any or all of them could have made mistakes, or have a significant bias, hence being referred to the original paper which should answer your questions about the methodology, “intent” or anything else. If they don’t then you can come back and ask specific questions about it, and the discussion might move on. You can’t expect people to spend their time rewriting the literature for you when they could point you to the primary sources.

Zachary
June 22, 2008

Dave Godfrey,

I don’t mean to step on your argument, but the citrate was not included in the medium as a control to test for contamination. The primary reason was as a chelating agent that allowed E. coli to take up iron from the medium. I go into this in a bit more detail, as well as the historical reasons for the relatively high citrate concentration in comment #115 above (which is a bit hard to read – I posted it before I realized that I needed spaces between paragraphs to make them stand out). Given the recent bent of the discussion here, you will likely find a number of things of interest in that comment (to say the least – and sadly, as I think you will agree).

Yours,
Zachary

Tulse
June 22, 2008

I did deal with methodological issues — I said that I assumed that the purpose of the glucose cycling was to try to promote Cit+ evolution. And I have also said a zillion times that Cit+ evolution could have been a goal or a hoped-for or wished-for result even if nothing specific had been done to favor Cit+ evolution.

Right, but why does it matter what the “hoped-for” or “wished-for” result was? If you think the methodology biased the result, then all this juvenile nattering about the definition of “goal”, and whether a particular result was “hoped-for” is just foolish, and completely irrelevant to the scientific question of how the bacteria evolved this trait.

In science, intention doesn’t matter, methodology does. As long as you trust the researchers to report their activities accurately, their “goals” in doing a particular experiment don’t matter. I honestly have no idea why you are so hung up on this issue, rather than actually focussing on the science.

Dave Godfrey
June 22, 2008

Thanks for the correction Zachary, one of the problems with long threads like this is that important pieces of information like that get missed.

Zachary
June 22, 2008

Dave Godfrey,

No problem. At this point, one of the reasons why I am working on a long post for Carl is so that most of the information I have posted (along with a lot else besides) can be collected in one place.

Carl, if you are reading this, thanks for your patience with me on getting it together!

Zachary

Hoovooloo
June 22, 2008

“For example, Zachary’s interpretation of the word “goal” might be different from my interpretation of the word — your interpretation and my interpretation of the word are certainly vastly different!”

Yes, but you yet again miss my point. You are trying to show that the paper lacks credibility. To do that, you will need to show that their methodology was flawed. Even if you can show that Cit+ was a “hoped for” result, that indicates nothing about the methodology. So please, stop trying to claim that Cit+ was a “hoped for” or “wished for” or “goal” (by your definition), as even if you are correct (which I dispute), it provides no evidence for your other claims (such as Zachary’s contradiction.

“That is not a direct answer to the question!”

Okay, look to post 270, where an Zachary explains what the purpose of the citrate is (spoiler: it’s not to evolve Cit+ bacteria).

“You don’t always cite the literature to show that there is scientific reasoning behind your claims.”

But I will either cite references, or step slowly and carefully through the logic that led to my conclusions, whereas you just claim things are “obvious” or that you simply assumed facts that led to your conclusion.

“If he won’t give straight answers to my questions, he is no better than a liar.”

Unless, of course, he does not want to respond to an obviously hostile, biased, random individual on the Internet, in which case I would call him “smart.”

“Something was done that favored Cit+ evolution: the glucose cycling.”

As I and others have explained, glucose cycling did not favor Cit+ bacteria, no more so than it favored bacteria that could digest other bacteria (I will respond preemptively to your tired excuse that cannibalism is more difficult than Cit+ by pointing out that Cit+ is a much more complex trait than more efficient glucose digestion or faster reproduction).

“If it was an intended purpose”

Weren’t you the one that asked where this intent “shit” came from? Regardless, you have been claiming that Zachary contradicted himself because you assumed Cit+ was the goal of the glucose cycling. You admit that glucose cycling would make it harder to evolve Cit+. As I pointed out above, that an evolved trait fits the environment is not evidence that the environment was designed for said trait. Until you provide evidence beyond the fact that Cit+ evolved, you have not shown that Cit+ was an intended purpose, and thus no contradiction.

“”Intent” is not an appropriate part of the definition of “goal.””

Did you also happen to notice that Webster defines a goal for sports and a goal for actions differently? And how about my example test cure for Alzheimer, where curing cancer was a possible and desirable result, but the experiment was not created with that purpose (goal)? It would seem to not only counter your example, but use a more appropriate definition of “goal” (purpose). Remember, to claim Zachary contradicted himself, you need to show that Cit+ was the purpose of the experiment.

“”I’m always kicking their butts — that’s why they don’t like me.””

Putting it in quotes doesn’t make it true.

Larry Fafarman
June 22, 2008

It is obvious that Zachary is ignoring the very reasonable questions I have here. He has no credibility.

Dave Godfrey said (#269) —

Larry, the experiment was performed to see what happens to E. coli when put on a starvation diet for a very long period of time. One of the easiest ways of doing this is glucose cycling.

As I said googolplex times, the glucose cycling favors Cit+ evolution by (1) allowing “silent” mutations during reproduction of the Cit- bacteria during glucose feeding and (2) giving Cit+ bacteria a reproductive advantage during glucose starvation. So I asked if favoring Cit+ evolution was a purpose of the glucose cycling and I got no answer.

Cit+ was one way the bacteria could evolve. But it wasn’t considered particularly likely

Let’s cut this bullshit about what the word “goal” means. The applicable definition in my printed dictionary is, “an object or end that one strives to attain.” The likelihood of attaining the goal has nothing to do with it — a long-shot goal is still a goal. If one is searching for the Holy Grail, the Lost Dutchman Mine, or the ivory-billed woodpecker, then finding those things are “goals.” “Intent” has nothing to do with it — a sports team “tries” to score a goal, not “intends” to score a goal. The cooperativeness of the bacteria has nothing to do with it — in sports, teams actually try to prevent the opposing teams from scoring goals, let alone try to help the opposing team score goals. So — Zachary said in comment #115 that it was his understanding that Cit+ evolution was an original goal of the experiment:

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding – I will need to check with him to make certain I understand this properly).

But then he immediately contradicted himself by saying that Cit+ evolution was never a goal —

the intent of the experiment was never to evolve a Cit+ E. coli variant (comment #115)

Also, he waffled in comment #122 —

The evolution of a citrate-utilizing variant E. coli was seen from the beginning as a possible occurrence, and one that would be pretty neat should it occur (and indeed as it has proven to be now that it has happened), but not a goal. (emphasis added) (comment #122)

His statement in #122 shows that he does not understand what the word “goal” means, so how could his statement that Cit+ evolution was not a goal be an acceptable answer to my question of whether a purpose of the glucose cycling was to favor Cit+ evolution? And he never answered that question — Hoovooloo just picked that statement as an answer to my question.

You’ve cited three review articles. None of them are original research.

Where did you pick up that term “original research” — from Wikipedia? According to the rules of Wickedpedia, if one reliable non-partisan source says that bears are always shitting and another reliable non-partisan source says that bears live in the woods, saying that bears shit in the woods is “original research” and is therefore not allowed. I am NOT exaggerating.

Anyway, as I said, instead of playing games by forcing me to guess answers according to indirect hints and semantics, why not just give me direct, unambiguous answers and clear up misunderstandings if they occur? What in the hell do you think this is, a charade? (oh, wait, maybe it is)

Hoovooloo moaned (#274) —

You are trying to show that the paper lacks credibility.

If the principal researcher lacks credibility, then the paper lacks credibility.

But I will either cite references, or step slowly and carefully through the logic that led to my conclusions, whereas you just claim things are “obvious” or that you simply assumed facts that led to your conclusion.

You are so full of living crap that it is coming out of your ears.

Unless, of course, he does not want to respond to an obviously hostile, biased, random individual on the Internet

I didn’t become hostile until after he started stonewalling my questions. And my alleged bias is not an excuse to not answer my reasonable questions.

As I and others have explained, glucose cycling did not favor Cit+ bacteria

you have been claiming that Zachary contradicted himself because you assumed Cit+ was the goal of the glucose cycling.

There was not only that — there was also Zachary’s statement that indicated that Cit+ evolution was a goal of the experiment, a statement that he later contradicted (see above quotes of comments #115 and #122).

You admit that glucose cycling would make it harder to evolve Cit+.

No, I never admitted that and my opinion is the opposite.

you have not shown that Cit+ was an intended purpose

As I pointed out, “intent” is irrelevant here.

And how about my example test cure for Alzheimer, where curing cancer was a possible and desirable result, but the experiment was not created with that purpose (goal)?

If curing cancer was foreseen as a possible result (it is obviously a desirable one), then it was one of the goals of the experiment. An experiment can have more than one goal, and a goal can be a secondary goal. And as I said, a goal can be a long-shot.

Putting it in quotes doesn’t make it true.

It doesn’t make it false, either.

Here is another one:

“So I’m the bad guy. How did that happen?”
— D-Fens in the movie “Falling Down”

That has nothing to do with glucose cycling-silent mutations are due simply to errors during reproduction. Thus, by reducing the amount of time the bacteria has to reproduce, glucose cycling would make it more difficult to evolve Cit+. Glucose cycling, and the effect it has on silent mutations (which you have twice said you agree with), is BAD for evolving Cit+, and thus was clearly not “striving to attain” Cit+ bacteria.

No, reproductive advantage would be determined by the presence of citrate. Had there been glucose the entire time and Cit+ evolved, the Cit+ would still flourish by consuming the citrate, while the Cit- would continue to consume the glucose. If you want to argue an environmental factor that allowed Cit+ to flourish, it would be the citrate.

“The applicable definition in my printed dictionary is, “an object or end that one strives to attain.””

Note the “strives to attain” portion. Just because something could happen, and would be nice if it did, does not mean the people have to strive to attain that result. For example, say the military wants to develop a new weapon that causes cancer, with no other effects. Of course, there is a chance that their weapon will accidentally cure cancer. If one of the researchers has a relative who has cancer, it is obvious that finding a cure for cancer would be a desirable result. Now, these two results (curing cancer and causing cancer) are mutually exclusive, so they can only strive to attain one of them. Thus, possibility and desire is not enough to define a goal, nor is it enough to find a problem with experimental methodology. Of course, you could claim that curing cancer would not really be desirable in this case, but then you are qualifying desire with what the goal of the experiment was, thus creating a circular definition.

“a long-shot goal is still a goal.”

What we are arguing is that you have not shown that Cit+ was a goal, not that you have shown it was a long-shot goal. The reason that probabilities came into this is that you claim that cannibalistic bacteria were a goal, on the grounds that they are so unlikely. You are the one that seems to believe a long-shot goal (under your definition) is not a goal.

“a sports team “tries” to score a goal.”

A “goal” in scoring in sports and a goal as it is normally used are different definitions. Look at this sentence, “Their goal is to score a goal.” Makes sense, doesn’t it? Now let’s plug in your definition, “Their possible and desirable result is to score a possible and desirable result.” Even to a child, it should be clear that the word “goal” has two different, yet common, definitions when used in the first sentence. Thus, drop the stupid sports analogy, unless your goal is to cause confusion.

“Zachary said in comment #115 that it was his understanding that Cit+ evolution was an original goal”

No, you redefined the word “goal” so that you can claim Cit+ was a “goal” of the experiment. If Zachary is using the common definition of the word goal, as defined in your dictionary, then you have to show they strived to attain Cit+ E. coli in order to claim their was a contradiction, which you have not done. Thus, Zachary has not contradicted himself.

“But then he immediately contradicted himself by saying that Cit+ evolution was never a goal –”

Only a contradiction if we use your bizarre, uncommon use of the word “goal.” Also, you use the word “goal” in two different ways. On one hand, you claim that a goal is just a desirable, possible result. However, when you claim that Cit+ was a goal of the experiment, and thus the experimental methodology is flawed, you are saying that Cit+ was what the experiment was striving to attain. Thus, “goal” in that situation means the result that the experiment is striving to attain. Your use of two very different definitions interchangeably is the source of confusion in this thread–not Zachary.

This shows a remarkable misunderstanding of science. The credibility of the paper is based on the experimental methodology ONLY. Just because a researcher has a bias, if that bias did not influence the experiment, the experiment’s results are still valid. So, to disprove the paper, you must show flaws in the methodology.

“You are so full of living crap that it is coming out of your ears.”

Yet you still refuse to provide any examples.

“my alleged bias is not an excuse to not answer my reasonable questions.”

Unless your (admitted) bias is skewing your view of the questions, so they only appear reasonable to someone with the same bias.

Sigh. You have been arguing that the experiment was designed to evolve Cit+ bacteria. Thus, once Cit+ bacteria evolved, the goal would be reached. What happens with the Cit+ after that point does not relate to the “goal” that you claim existed. Hence, even if the glucose cycling provided a reproductive advantage to Cit+ bacteria, this would only occur AFTER the Cit+ has evolved, and thus in no way relates directly to the “goal.” As you agreed (post 256) that glucose cycling would work to reduce silent mutations, and since Cit+ reproductive rates do not matter in terms of evolving Cit+ (as Cit+ would not yet exist), you have admitted that glucose cycling works against Cit+ mutation.

“As I pointed out, “intent” is irrelevant here.”

Not if you want to discredit the paper, it isn’t.

“”So I’m the bad guy. How did that happen?””

By being a willfully ignorant wannabe biologist who is the laughingstock of this blog. Oh, and you might want to look for some new quotes, King Lear, Schwarzenegger and “Falling Down” are getting old.

emc
June 22, 2008

D-Fens in the movie “Falling Down” suffered a nervous breakdown, during which he committed a host of violent crimes.

Prior to his breakdown, he was a control freak and abusive asshole, leading to his divorce and loss of contact with his daughter. His dysfunctional personality probably caused the loss of his job, which may have precipitated his breakdown.

I wonder if Larry has the sense to realize that this quote was not made by a sane, sensible person who was being unduly oppressed by authorities.

– emc

Dave Godfrey
June 22, 2008

Larry, it seems fairly clear to me (from what Zachary says in post 122) that Cit+ was not the aim of the experiment, merely a postulated outcome. “The evolution of Cit+ in one of the twelve populations has opened new areas of inquiry in the experiment, but the experiment was never designed to bank on the evolution of that one novel trait.”

As I understand it (and I’m sure Zachary will be able to correct me), he was unclear as to whether Dr Lenski thought that the bacteria might evolve Cit+ at the beginning of the experiment. Given that only one or two other examples of Cit+ in E. coli have been seen otherwise the thought that Cit+ might evolve may not have crossed his mind.

To apply the sports analogy again, if one of the teams was kidnapped by aliens and thereby forfeited the match this would be a “goal” by your definition. (After all the other team want to win). Its unlikely, but because it means the other team wins its a “long-shot goal”.

Had there been glucose the entire time and Cit+ evolved, the Cit+ would still flourish by consuming the citrate, while the Cit- would continue to consume the glucose.

But if there is glucose the entire time, the Cit+ bacteria have no advantage over the Cit- bacteria so far as the availability of food is concerned. However, during glucose starvation, the Cit+ bacteria have an advantage because they can continue to reproduce while the Cit- bacteria cannot. I have stated this many times and it is self-evident. Not only do you have the reasoning ability of a two-year-old, but you can’t remember anything.

What we are arguing is that you have not shown that Cit+ was a goal

I am not trying to show that Cit+ evolution was a goal — I am trying to find out if it was a goal.

“But then he immediately contradicted himself by saying that Cit+ evolution was never a goal –“
Only a contradiction if we use your bizarre, uncommon use of the word “goal.”

I use the word “goal” the same way that normal, sane people use the word.

On one hand, you claim that a goal is just a desirable, possible result.

Nope, I didn’t say that. I said that a goal is something foreseen as a desirable, possible result of an effort (“effort” was often implicit because I was talking about the experiment or other efforts).

when you claim that Cit+ was a goal of the experiment

As I said, I am not claiming that — that is something I am trying to find out.

The credibility of the paper is based on the experimental methodology ONLY.

Why should I trust a paper written by a known liar like Zachary?

You have been arguing that the experiment was designed to evolve Cit+ bacteria.

I am arguing that only in the sense that it appears that a purpose of the glucose cycling was to favor Cit+ evolution. I am trying to find out if that was the case or if Cit+ evolution was a goal even if that was not the case.

Thus, once Cit+ bacteria evolved, the goal would be reached.

Even after the Cit+ bacteria evolved, there would be other reasons to continue the experiment, e.g., (1) to test for historical contingency, (2) to see if C+ bacteria evolve in any of the other 11 lines, and (3) to see if better Cit+ bacteria evolve (this happened — the Cit+ bacteria that evolved after 33,000 generations became more predominant than the Cit+ bacteria that evolved at 31,500 generations).

you have admitted that glucose cycling works against Cit+ mutation.

Again, I have never admitted that and I claim the opposite. The glucose starvation tends to reduce the silent mutations in the Cit- bacteria but gives a tremendous advantage to Cit+ bacteria, and the overall effect on Cit+ evolution is positive.

By being a willfully ignorant wannabe biologist who is the laughingstock of this blog.

You and your fellow trolls are the laughingstocks.

King Lear, Schwarzenegger and “Falling Down” are getting old.

Getting old? I have used quotes from them sparingly.

Larry Fafarman
June 22, 2008

Dave Godfrey said,

Larry, it seems fairly clear to me (from what Zachary says in post 122) that Cit+ was not the aim of the experiment, merely a postulated outcome. “The evolution of Cit+ in one of the twelve populations has opened new areas of inquiry in the experiment, but the experiment was never designed to bank on the evolution of that one novel trait.”

Sigh. I would like to know all the goals of the experiment, but right now I am just trying to find out whether Cit+ evolution was a goal, even if it was not the sole goal or a main goal. Zachary created confusion here with his mutually contradictory statements about whether Cit+ evolution was a goal of the experiment. I am using the plain, everyday meaning of “goal.” If one is searching for the Ring of the Nibelungs or the ivory-billed woodpecker, finding them is a “goal.” And I am also trying to find out if the purpose or one of the purposes of the glucose cycling was to favor Cit+ evolution.

Compare my modest requests for information to Andy Schlafly’s request for all of the raw data (Schlafly is the founder of Conservapedia). Anyway, Schlafly doesn’t need the raw data to discredit the paper — I have already done that job for him.

emc:

I wonder if Larry has the sense to realize that this quote was not made by a sane, sensible person who was being unduly oppressed by authorities.

On the contrary, I think that the movie tried to portray D-Fens as the only sensible person around. Anyway, the quote is appropriate here.

emc
June 23, 2008

“On the contrary, I think that the movie tried to portray D-Fens as the only sensible person around. Anyway, the quote is appropriate here.” – Larry

“Some statements are so stupid, all you can do is underline them.” – Christopher Hitchens

Indeed.

– emc

Cynthia Wood
June 23, 2008

On the contrary, I think that the movie tried to portray D-Fens as the only sensible person around.

Well. That just told heaps about your views of the world I really didn’t want to know, Larry.

Good luck with that life thing. I hope to God you don’t live anywhere near me.

Hoovooloo
June 23, 2008

I had a methodical, traditional response to your last post typed out. However, I realized that writing a long, comprehensive response only gives you an opportunity to ignore my most important points. So, this post will be my brief attempt to show why your evidence fails. Likewise, for brevity, I will not include quotations here (as I have made all these points, with quotes, in the past).

Mr. Farfaman, you have claimed that you are trying to show the paper lacks credibility. As science is (ideally) free of personal bias, you must show an error in the experiment’s methodology to truly discredit the paper. To that end, you have repeatedly claimed that glucose cycling somehow helped Cit+ evolve, beyond what might happen in nature. You base this claim on two ideas: That glucose cycling allows silent mutations during the feeding phase, and that glucose starvation grants Cit+ bacteria a reproductive advantage. I will deal with both of these claims in turn, but remember, during all of this we will be comparing this experiment to what might happen in nature, as if Cit+ was about as likely to evolve in the lab as in a possible natural situation, the results hold as credible.

Your first claim, that feeding during the glucose cycling allows silent mutations necessary for Cit+, has been the subject of much of our discussion. You do not believe a cycling situation could occur in nature, and thus, by your logic, for E. coli to survive the only possible habitats are ones that have a plentiful glucose supply. Glucose, as a sugar, is not a mutagen. Thus, the glucose itself will not directly effect the probability of a silent mutation occurring during any reproductive cycle, only the number of reproductive cycles that can take place in a given time period (in this case, a day). Glucose cycling, then, reduces the number of reproductive cycles that can occur each day, making it take longer, on average, for the silent mutation necessary for Cit+ to occur (as compared to plentiful glucose). With this you have agreed in past posts. In light of this, you claim that the reproductive advantage given to Cit+ during the starvation phase more than makes up for this fact. However, keep in mind that glucose starvation makes it more difficult to see Cit+ evolve in the lab than had plentiful glucose been used.

Now on to the effect starvation would have on Cit+ evolution. Remember, to discredit the paper, you must show that it was significantly more likely for Cit+ to evolve in the experiment than in nature. The initial mutations are silent, so by definition they have no observable effect on the bacteria with the mutation versus their neighbors. Thus, the amount of food will have no effect in favor of Cit+ mutants at this stage. Now, the other food source was citrate. For the lack of glucose to provide a reproductive advantage to a bacteria, the bacteria must either outcompete the other bacteria for the glucose, or find a new food source. Remember, we are discussing if the experiment made it easier for Cit+ to evolve in the lab than in nature. Since the Cit+ bacteria, as described in the paper, did not appear to have any visible mutations between the initial silent mutation(s) and the ability to digest citrate, then there was no chance for any food sources to influence the evolution other than the citrate itself. Of course, for the bacteria to be affected by the citrate in terms of reproduction, they must already be able to digest citrate. Since the question is whether the experiment made it unreasonably easy for the bacteria to evolve Cit+ in the first place, the effects of glucose cycling, and the citrate, become unimportant once Cit+ has first appeared in a single bacterium.

While the abundance of citrate during periods of glucose starvation may allow the Cit+ bacteria to reproduce rapidly once it has evolved, and thus quickly become visible, it does not effect the likelihood of Cit+ occurring in the first place. Since the question was how glucose cycling effects the evolution of Cit+ in the experiment versus the lab, and answer is either not at all or by making it more difficult, it should be clear to you that glucose cycling does not promote Cit+ evolution.

Of course, you can try to claim that the paper is not a credible source of data. However, your reason for doubting the paper is that you believe that glucose cycling, as described by Zachary and the paper, promotes Cit+ evolution. Thus, in calling the paper lacking in credibility, your are in fact admitting that your own evidence for its lack of credibility lacks credibility, providing an interesting paradox.

Larry Fafarman
June 23, 2008

Hoovooloo says,

So, this post will be my brief attempt to show why your evidence fails.

You call your post “brief”? LOL

Mr. Farfaman, you have claimed that you are trying to show the paper lacks credibility. As science is (ideally) free of personal bias, you must show an error in the experiment’s methodology to truly discredit the paper.

My reason for saying that the paper lacks credibility is the principal investigator’s failure to answer my simple, basic questions about it. Your comment does not address that issue, and your comment addresses issues I never raised, e.g., whether or not the experiment simulates nature. I will, however, address one of the issues that you raised:

While the abundance of citrate during periods of glucose starvation may allow the Cit+ bacteria to reproduce rapidly once it has evolved, and thus quickly become visible, it does not effect the likelihood of Cit+ occurring in the first place.

The rapid reproduction of the Cit+ bacteria during glucose starvation, while the Cit- bacteria cannot reproduce, is part of Cit+ evolution and part of evolution of E. coli bacteria in general, and not something that occurs after Cit+ evolution. This is “artificial” selection, the equivalent of natural selection in nature.

emc driveled,

“On the contrary, I think that the movie tried to portray D-Fens as the only sensible person around. Anyway, the quote is appropriate here.” – Larry
“Some statements are so stupid, all you can do is underline them.” — Christopher Hitchens

You can interpret the movie your way and I will interpret it my way. To me, D-Fens was reacting to injustice, intolerance, wastefulness, and the petty ways in which people mistreated him. The plot of the movie is here —http://en.wikipedia.org/wiki/Falling_Down

Trevor Murray
June 23, 2008

Yes D-Fens was reacting to those things, however the way he reacted was unacceptable for the types of society we live in (Criminal offences in fact). Doing bad things for good reasons doesn’t change the fact that their bad things. At the end of the movie D-fens realises that, and thus the quote. In doing so he realises the only way he can make up for his mistakes was to ensure he gets shot to make sure his family get the insurance. His final act was one of self sacrifice all those leading up were merely criminal.

Dave Godfrey
June 23, 2008

From everything I’ve seen Zachary write, I can only conclude that Cit+ evolution was not a deliberate aim (“goal”) of the experiment.

It was an event that Lenski may (or may not- Zachary is unclear on this point- and this point alone) have predicted as a possible outcome, along with any number of other traits that they may or may not have seen.

From the paper itself: “To address the repeatability of evolutionary trajectories and outcomes,the long-term evolution experiment (LTEE) with Escherichia coli was started in 1988 with the founding of 12 populations from the same clone.”

“The founding strain is strictly asexual, and thus
populations have evolved by natural selection and genetic drift acting on variation generated solely by spontaneous mutations that occurred during the experiment. Thus, the LTEE allows us to examine the effects of contingency that are inherent to the core evolutionary processes of mutation, selection, and drift.”

The experiment’s stated aim is to investigate patterns of convergent and contingent evolution. There appears to be lots of convergence in the populations (evolution of large cell size, increased growth rates, DNA supercoiling, etc.)

Larry Fafarman
June 23, 2008

David Godfrey said (#286) —

From everything I’ve seen Zachary write, I can only conclude that Cit+ evolution was not a deliberate aim (“goal”) of the experiment.

“Everything”? What about this statement (from comment #115) —

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding – I will need to check with him to make certain I understand this properly).

David said (#286) —

It was an event that Lenski may (or may not– Zachary is unclear on this point — and this point alone) have predicted as a possible outcome, along with any number of other traits that they may or may not have seen.

Sheeeesh — many if not most people interpret the word “goal” as meaning something foreseen as a possible and desirable result of an effort, so if you don’t want to be misunderstood, you should not use the word to mean something else.

And since Zachary is unclear on this point, why hasn’t he clarified himself?

Trevor Murray said (#285) —

Doing bad things for good reasons doesn’t change the fact that their (sic) bad things. At the end of the movie D-fens realises that, and thus the quote.

I don’t see how you can possibly make that interpretation. To me, his statement “How did that happen?” following “So I’m the bad guy?” showed that he was bewildered that he was regarded as the bad guy and that he felt that he was really the good guy while others were the bad guys and that he felt he was justified in doing what he did. And what he did was not always criminal — for example, he legitimately acted in self-defense when the gang members threatened him in the park. Anyway, as I said, others can interpret the movie their way and I will interpret it my way.

Josh
June 23, 2008

Larry,

Got a new quote to attach to your comments:

“The definition of insanity is doing the same thing over and over again and expecting different result “

Hoovooloo
June 23, 2008

“My reason for saying that the paper lacks credibility is the principal investigator’s failure to answer my simple, basic questions about it. Your comment does not address that issue, and your comment addresses issues I never raised, e.g., whether or not the experiment simulates nature.”

Clearly, you do not understand how science works. As I and others have pointed out, regardless of the personal feelings and biases of the researchers, if you cannot find a point where the paper is not a reasonable simulation of nature, a flaw in the methodology, you cannot say that the results are not a credible example of what is naturally possible. Until you realize Zachary’s quotes and actions alone are not enough to discredit the paper, no one here will take what you have to say seriously. In light of that, if you want to discredit the paper scientifically, in terms of Cit+ evolution, you must show that something in their methodology effected the INITIAL evolution of Cit+ in such a way that it could not happen in nature.

“The rapid reproduction of the Cit+ bacteria during glucose starvation, while the Cit- bacteria cannot reproduce, is part of Cit+ evolution and part of evolution of E. coli bacteria in general, and not something that occurs after Cit+ evolution.”

No. The rapid reproduction of Cit+ bacteria only occurs after Cit+ has evolved. After all, how could the glucose cycling give a reproductive advantage to something that does not yet exist? Admittedly, it will influence the continued evolution of Cit+ and thus the E. coli in general, but if the question is the effects on the initial mutation, the first bacteria that could digest Cit+ and thus the first bacteria that could have an advantage during periods of glucose starvation, the answer is that it did not effect it, at least not in a positive manner. Unless how you can explain how glucose starvation gave a reproductive advantage to bacteria that could NOT digest citrate, but have the silent mutation, then you have no evidence that glucose cycling helped Cit+ evolve initially.

Larry Fafarman
June 23, 2008

Larry,

Got a new quote to attach to your comments:

“The definition of insanity is doing the same thing over and over again and expecting different result “

Is that just another way of saying that I am wasting my time trying to drum some common sense into other commenters here?

Dave Godfrey
June 23, 2008

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit, thereby presenting a potential point of divergence between the populations (this is my understanding – I will need to check with him to make certain I understand this properly).

And this is the only point that Zachary is unclear on. Whether or not at the start of the experiment Lenski thought that Cit+ might evolve. He doesn’t need to clarify himself because it really isn’t important which features Lenksi thought might evolve, thinking something won’t make it happen.

From #122

The evolution of a citrate-utilizing variant E. coli was seen from the beginning as a possible occurrence, and one that would be pretty neat should it occur (and indeed as it has proven to be now that it has happened), but not a goal.

That sounds to me like a clarification. Evolving Cit+ wasn’t the aim of the experiment, but was postulated as a possible outcome. It is two different things. If you went looking for the Ivory-Billed Woodpecker, but also found your keys then would that be a goal? And if not why not?

Trevor Murray
June 23, 2008

Oh so D-fens actions were ok becuaes they were only somtimes criminal?

W. Kevin Vicklund
June 23, 2008

Sheeeesh — many if not most people interpret the word “goal” as meaning something foreseen as a possible and desirable result of an effort, so if you don’t want to be misunderstood, you should not use the word to mean something else.

But you’re wrong. Most people do not interpret the word “goal” to mean that. In addition to the aspects you mentioned above, they also include an aim – a purpose, a direction, an intent – that guides that effort. The reason you’re misunderstood is because you, not Zachary or the half dozen people here participating in this portion of the argument(“we”), are not using the word in its common meaning.

Here’s the definitions of several words taken from a famous dictionary. Irrelevant definitions have been removed and synonyms have been highlighted:

goal

2: the end toward which effort is directed : aim

synonyms see intention

intent

1 a: the act or fact of intending : purpose; especially : the design or purpose to commit a wrongful or criminal act (admitted wounding him with intent) b: the state of mind with which an act is done : volition
2: a usually clearly formulated or planned intention : aim (the director’s intent)
3 a: meaning, significance b: connotation 3

synonyms see intention

intend

1: to direct the mind on
3 a: signify, mean b: to refer to
4 a: to have in mind as a purpose or goal : plan b: to design for a specified use or future

The definition of goal (“the end toward which effort is directed”) and definition 4a of intend (“to have in mind as a purpose or goal”) are of particular interest, as they not only support the interpretation of “goal” that we have been using, but demolish your objection to the use of “intend” as a component of “goal”.

From the same source, I now include “intention” (which “goal” and “intent” list as a synonym). Of particular interest is the long discussion it goes into on the connotations of its various synonyms.

intention

1: a determination to act in a certain way : resolve
3 a: what one intends to do or bring about b: the object for which a prayer, mass, or pious act is offered

synonyms intention, intent, purpose, design, aim, end, object, objective, goal mean what one intends to accomplish or attain. intention implies little more than what one has in mind to do or bring about announced his intention to marry. intent suggests clearer formulation or greater deliberateness the clear intent of the statute. purpose suggests a more settled determination being successful was her purpose in life. design implies a more carefully calculated plan the order of events came by accident, not design. aim adds to these implications of effort directed toward attaining or accomplishing her aim was to raise film to an art form. end stresses the intended effect of action often in distinction or contrast to the action or means as such willing to use any means to achieve his end. object may equal end but more often applies to a more individually determined wish or need his constant object was the achievement of pleasure. objective implies something tangible and immediately attainable their objective is to seize the oil fields. goal suggests something attained only by prolonged effort and hardship worked years to reach her goals.

The basic meaning (common definition) of all of those synonyms is given followed by the specific connotation (the implied meaning). Therefore, goal is here defined as “what one intends to accomplish or attain” with the implication that it is “something attained only by prolonged effort and hardship”. Larry is trying to argue that only the second part applies, but clearly the dictionary requires that the first part, the basic meaning, also applies.

Oh, and the dictionary in question? The Merriam-Webster Online Dictionary, which is the latest edition of Larry’s preferred dictionary. It also happens to be nearly identical to my 9th Collegiate print edition.

Of course, all of this is unecessary. Laryy’s objections to the use of “intent” are merely post-hoc rationalizations designed to avoid admitting a mistake or misunderstanding, rather than a principled stand on what he thinks intent means.

You see, Larry’s original claim that Zachary was making contradictory statements was based on Zachary’s use of “intent”, not “goal”, and Larry clearly understood how the word was being used.

Zachary,

The following comments/questions are about the statements highlighted above.

The following two statements are contradictory —

When Dr. Lenski started, he figured the citrate would provide an opportunity that the populations might or might not figure out a way to exploit

— and —

the intent of the experiment was never to evolve a Cit+ E. coli variant

I thought that the purpose of the experiment was to try to evolve a Cit+ mutant by giving the bacteria lots of citrate to eat and little glucose to eat in order to give a Cit+ mutant a big advantage.

If Larry actually believed that “intent” meant what he now says he believes it means, he wouldn’t have made the claim that the statements are contradictory. After all, under his claimed definition, one can’t have complete control over the outcome of the experiment, and therefore the two statements would not conflict.

But Larry went further than that. In the follow-up sentence, he makes it explicit that he interprets “the intent of the experiment was never to evolve a Cit+ E. coli variant” to mean the opposite of “the purpose of the experiment was to evolve a Cit+ mutant”. When Zachary followed up by clarifying what he meant by “figured” and “intent”, Larry attacked his definition of “goal”. Since Larry has already demonstrated that he is lying about what he understands “intent” to mean, it is not unreasonable to conclude that he is also lying about what he believes “goal” means in order to avoid admitting that he made a mistake. I should further note that Larry’s statement also proves that he understood that if the intent was not to evolve a Cit+ mutant, then the purpose of the glucose cycling could not be trying to evolve a Cit+ mutant.

Larry Fafarman
June 23, 2008

The trolls are really out in force today.

Hoovooloo said (comment #289) —

“The rapid reproduction of the Cit+ bacteria during glucose starvation, while the Cit- bacteria cannot reproduce, is part of Cit+ evolution and part of evolution of E. coli bacteria in general, and not something that occurs after Cit+ evolution.”
No. The rapid reproduction of Cit+ bacteria only occurs after Cit+ has evolved.

Wrong. As I explained, the rapid reproduction of Cit+ bacteria during glucose starvation, at a time when the Cit- bacteria cannot reproduce, is the phase of evolution called selection — natural selection in the wild and artificial selection in the lab.

Dave Godfrey said (comment #291) —

And this is the only point that Zachary is unclear on.

Wrong — he also did not answer the question of whether favoring Cit+ evolution was a purpose or one of the purposes of the glucose cycling. So why doesn’t he clear up these points?

He doesn’t need to clarify himself because it really isn’t important which features Lenksi thought might evolve, thinking something won’t make it happen.

Understanding the goals and purposes is necessary for understanding the experiment.

Evolving Cit+ wasn’t the aim of the experiment, but was postulated as a possible outcome. It is two different things.

So maybe it could be called a secondary goal — but it is still a goal. An experiment can have more than one goal. You are playing word games.

If you went looking for the Ivory-Billed Woodpecker, but also found your keys then would that be a goal?

If finding the keys is foreseen as a possible and desirable outcome of the search, then finding the keys would be a goal. You are making this much too complicated.

Trevor Murray said (comment #292) —

Oh so D-fens actions were ok becuaes they were only somtimes criminal?

Your problem is that you are interpreting a movie too literally — it is just a movie and was intended to be entertaining. For example, D-Fens’ damage to the convenience store’s merchandise was technically illegal, but the store-owner got what was coming to him. D-Fens had asked him for a dollar’s change to make a telephone call and the store-owner insisted that D-Fens make a purchase. D-Fens tried to purchase a can of soda but was told that the price was 85 cents, not leaving enough change to make a phone call. The detective who came to investigate said in amazement, “you mean that he actually paid for the soda?”

Pettifogger Kevin Vicklund said (comment #293) —

Most people do not interpret the word “goal” to mean that.

Kevin, you are making this much too complicated. My printed dictionary’s applicable definition of “goal” is “an object or end that one strives to attain.” Conducting the experiment is an act of striving and the glucose cycling is another act of striving. This definition might not be the only definition of “goal” but it is an accepted definition. I pointed out that confusion resulted from Zachary’s use of the word “goal” and he made no attempt to clear up the confusion.

I think that maybe I will take Josh’s advice and stop my futile efforts to try to drum some common sense into other commenters.

W. Kevin Vicklund
June 23, 2008

Larry, do you drive a Honda?

W. Kevin Vicklund
June 23, 2008

(bear with me, this actually has a purpose)

John
June 23, 2008

I read through the papers Zachary mentioned that talk about the goals and objectives of the experiment. None mention Cit+. You would know this if you had bothered to check them. He was reasonable in what he said, and honest. No reasonable person would see a contradiction in what he said, and a reasonable person with unanswered questions would read the papers. The contradiction is in your mind only. No reasonable person would twist the English language like you do. You really don’t seem to understand what a goal is or how science works. If I were him, I wouldn’t reply to you either with how you treated him. You have been rude and slanderous toward him and everyone else here. Do you really behave this uncivilly like this in real life?

W. Kevin Vicklund
June 23, 2008

Put it this way, John. Larry perjured himself in Federal Court over a fee that he didn’t have to pay. He’s very much like the D-Fens character he identifies so much with; every little slight (real or perceived) is met with a disproportionate response.

Larry, on further thought, don’t answer that question. I’ll try to make my point in a less personal manner tomorrow evening.

Carl Zimmer
June 24, 2008

I think it may be time to rein this thread in. Larry claimed that he had found a huge flaw in the research I described, even though he had not yet read the paper because he has “other interests.” Other commenters have made clear that his claim of a flaw is groundless. Apparently Larry has only managed to “browse” the paper since then, but despite his other interests, he has fond the time to write dozens of posts accusing the authors of this study of duplicity. Meanwhile, totally unrelated topics such as Michael Douglas movies have moved into the thread as well. The shark has jumped, methinks.

W. Kevin Vicklund
June 24, 2008

Zachary, I have a question that I hope you can answer in your long post. If I understand the way the experiment is set up, the Cit+ sub-population of the Ara-3 line should deplete the broth of citrate by the time the next transfer occurs. Does the leveling off of the Cit+ growth in Fig.2 (at about 14 hours) correspond to the time of citrate depletion?

Zachary
June 24, 2008

W. Kevin Vicklund,

I had not thought to put that in the long post, which is likely too long as it stands, so I will answer here. The leveling off around 14 hours, which is referred to as the reaching of stationary phase of bacterial growth, may, to a first approximation, be considered when the citrate is exhausted. There are some caveats to that, however. The first is that we have not yet had the time to do the analysis of how the medium changes over time as the citrate is used up, so we don’t fully know just yet. The second is that the growth rate of Cit+ changes during the long, slow phase of growth after glucose runs out. If it is just growing on citrate during that time, then we would expect only a single growth rate. We think that it is possible that Cit+ may be spilling something into the medium while growing on citrate, and it then switches to growing on whatever that is when citrate runs out. If this is the case, then citrate is likely exhausted a bit before Cit+ hits stationary phase. When we get to the medium analysis, we can answer that question better. In any case, once they hit that leveling off, the Cit+ population is effectively without food any more, and end up starving until transfer.

The interesting thing is that, when Cit+ first evolved, the Cit+ variant was so poor at using citrate that very, very little of the citrate in the medium was actually used before the population was transferred. Indeed, I have done some growth studies with those very early Cit+ clones, and most of them won’t start growing quickly on citrate even after 72 hours when left in the same medium, and thus don’t come close to using up the citrate. It is going to take some more work to nail this down, but it looks like there were perhaps four to seven beneficial mutations that occurred in the Cit+ subpopulation between 31,500 and 33,000 generations. Each of these improved growth on citrate until the Cit+ variants arose that were strong enough to take over the population and cause the expansion demonstrated in figure 1. In short, Cit+ evolved to use all the citrate in the medium before the next transfer.

Larry Fafarman
June 24, 2008

Carl Zimmer said,

Larry claimed that he had found a huge flaw in the research I described, even though he had not yet read the paper because he has “other interests.”

I never claimed that I found a “huge flaw in the research” — I only complained about Zachary’s failure to give straight consistent answers here. In comment #150, I showed that he made confusing, inconsistent, ambiguous, and mutually contradictory statements here about whether Cit+ evolution was a “goal” (or a hoped-for result or a wished-for result or whatever) of the experiment. So I have been asking for a clarification which I have not gotten. And he has refused to answer my question of whether the purpose or one of the purposes of the glucose cycling (alternating glucose feeding and glucose starvation) was to favor Cit+ evolution.

Other commenters have made clear that his claim of a flaw is groundless.

Some of the other commenters agree or appear to agree with my charges against Zachary. For example, Dave Godfrey said (comment #291), “And this is the only point that Zachary is unclear on. Whether or not at the start of the experiment Lenski thought that Cit+ might evolve.” (and Zachary has also not answered my question about the purpose of the glucose cycling). Keiran Lerch said (comment #220), “To summarize, you can’t change the environment or the people in this particular discourse, but you can change yourself or alter your approach.” My approach has not been bad but I should be getting straight answers even if my approach were bad.

Meanwhile, totally unrelated topics such as Michael Douglas movies have moved into the thread as well.

All I did was just make a very apt brief quote from “Falling Down” (“So I’m the bad guy? How did that happen?”) and then others started a big argument over that. And now Kevin Vicklund is trying to start an argument over my lawsuits against California’s unconstitutional vehicle “smog impact fee.”

I would not have been so persistent in asking questions here if this paper had not attracted so much interest and controversy. The Internet has several reviews and hundreds of comments about the paper. Andy Schlafly of Conservapedia has even gone so far as to request the raw data of the experiment. Because of all this interest and controversy, I think that the paper’s authors should meet the highest standards of integrity, and Zachary has failed to do that here.

David Marjanović
June 24, 2008

Andy Schlafly of Conservapedia has even gone so far as to request the raw data of the experiment.

Read the Pharyngula post, and the comments on it, to learn how stupid this is.

Why do I have to wade through a lot of stuff unrelated to my questions?

It isn’t unrelated. It is necessary background — necessary for you to understand your own questions and the answers to them.

yet you think it is OK to just refer me to a long paper in answering my simple, specific questions.

Yes, it is in fact OK.

It is sometimes OK. It was not OK here.

Telling you to read the paper is always OK, because you are expected to do that anyway. Read the paper, and if you have any questions left then, then come back.

You folks have a double standard. You expect me to give direct answers to your questions but think that bibliography-bluffing is OK in responding to my questions.

Again, why should we bother? You must read the paper anyway.

“Just”? That requires a transporter protein. Why do you think that must be easy to evolve?

It is comparatively easy to evolve.

Why do you think so?

and now you are questioning whether that evolution is “desirable.”

It was not expected to happen. It was a surprise.

But if it was foreseen as a possible and desirable event, then it was a goal. If it was a goal but a long-shot goal, then it should be called a long-shot goal. Anyway, I proposed that we stop using the word “goal” here because you folks don’t understand the word’s meaning.

You are using it the wrong way. If it was foreseen as a possible and desirable event, then it was a possible and desirable outcome. Had Cit+ not evolved and the experiment therefore been considered a failure, then the evolution of Cit+ would have been a goal. When a goal is not attained, that’s a failure. If Cit+ had not evolved, that would not have been a failure; the goal was to watch natural selection in action, and that was reached.

But I have to repeat Tulse and many others: What does it matter if Cit+ evolution was a goal or not? The bacteria aren’t psychics, they didn’t care about the wishes of the experimenters.

No. The purpose was for glucose to be the limiting factor, so that higher efficiency of glucose metabolism would be selected for.

Selection for higher efficiency of glucose metabolism would occur without limiting the glucose supply.

No, why? A truly unlimited supply would not lead to such selection. Selection occurs for the growth-limiting factor.

I assert that it appears that the purpose or one of the purposes of giving an insufficient supply of glucose was to try to promote evolution of citrate-eating bacteria.

It wasn’t, but even if it was*, so what?

* That would be like putting your family underwater for a few hundred millennia and waiting for gills to grow.

How many times do I have to repeat myself? I said that the glucose cycling tends to reduce silent mutations because the bacteria that can eat only glucose cannot reproduce after the glucose supply is exhausted, and errors in gene duplication during reproduction are a major source of mutations. Suppose, for example, instead of starting new populations every day, the populations were kept for a year and were still given just a few hours of glucose supply. That would make it quite obvious that the glucose cycling tends to reduce silent mutations in the bacteria that can eat only glucose.

Why would that reduce silent mutations? It wouldn’t, because silent mutations are by definition silent, which means they are neutral — they don’t have any effect on the phenotype and therefore are neither beneficial nor detrimental, which means natural selection is completely blind to them. They absolutely don’t matter.

You linked to it in comment 155 and quoted it.
So how does the article misinterpret the experiment?

Here’s the quote again:

In 1988, Richard Lenski, Michigan State University, East Lansing, founded 12 cultures of E. coli and grew them in a laboratory, generation after generation, for twenty years (he deserves some marks for persistence!). The culture medium had a little glucose but lots more citrate, so once the microbes consumed the glucose, they would continue to grow only if they could evolve some way of using citrate. Lenski expected to see evolution in action.

This sounds like the bacteria were expected to eat the citrate. They weren’t. More importantly, it sounds like this was the whole point of the experiment. This is completely wrong. I’m really surprised you still haven’t noticed this.

The rest of your comment (#233) is a response to another commenter.

That’s why it’s separated by a line of ———.

You ought to identify who you are responding to so that people won’t think that you are responding to me (especially when your comment starts with responses to me). It is especiall annoying that some people may think that I made statements that another commenter made.

I am a scientist. I don’t respond to people, I respond to questions, statements, hypotheses. I respond to what people say. Who says it doesn’t matter; it has no effect on the credibility of what is said, for example.

Anyway, as I said, IMO we should stop using the term “goal” here because you folks can’t understand its meaning.

And it has never occurred to you that if 15 people agree with each other and disagree with you that perhaps you are the one who’s wrong?

David Marjanović
June 24, 2008

Oopsie. Some of the triple blockquotes in my last post didn’t work. But I think it’s pretty obvious who wrote what.

Dave Godfrey
June 24, 2008

I certainly don’t agree with you Larry. I can’t see that I appear to either. I quoted Zachary’s first comment to show the only point that he seemed to be unsure about, (whether Cit+ was postulated at the start) and then his subsequent comment where he corrects himself (yes, but its so rare that it really wasn’t expected).

Now can we please move on?

Zachary
June 24, 2008

Dave Godfrey,

I would also like to point out that I gave people information for publications (#145 and #147 on Dr. Lenski’s website) that describe the goals of the experiment so that my word wouldn’t have to be taken on the matter.

Zachary

Larry Fafarman
June 24, 2008

David Marjanović said (#303)–

Andy Schlafly of Conservapedia has even gone so far as to request the raw data of the experiment.
Read the Pharyngula post, and the comments on it, to learn how stupid this is.

I agree that it is stupid. So?

David Marjanović said (#306) —

Oopsie. Some of the triple blockquotes in my last post didn’t work. But I think it’s pretty obvious who wrote what.

No, it is not obvious who said what, and the problem of determining who said what is not just with the triple blockquotes.

David Marjanović said (#305) —

I said that the glucose cycling tends to reduce silent mutations because the bacteria that can eat only glucose cannot reproduce after the glucose supply is exhausted, and errors in gene duplication during reproduction are a major source of mutations.
Why would that reduce silent mutations?

The statement you quoted answers your question — silent mutations tend to be reduced because errors in gene duplication during reproduction are a major source of mutations, and Cit- bacteria cannot reproduce when there is no glucose to feed on.

Here’s the quote again (from comment #155)In 1988, Richard Lenski, Michigan State University, East Lansing, founded 12 cultures of E. coli and grew them in a laboratory, generation after generation, for twenty years (he deserves some marks for persistence!). The culture medium had a little glucose but lots more citrate, so once the microbes consumed the glucose, they would continue to grow only if they could evolve some way of using citrate. Lenski expected to see evolution in action. — fromhttp://creationontheweb.com/content/view/5827
This sounds like the bacteria were expected to eat the citrate. They weren’t. More importantly, it sounds like this was the whole point of the experiment. This is completely wrong. I’m really surprised you still haven’t noticed this.

I never said that Cit+ evolution was the whole point of the experiment. I quoted the above article just to show that others have the same impressions that I had — that Cit+ evolution was a goal of the experiment and that a purpose of the glucose cycling was to favor Cit+ evolution.

Dave Godfrey said (#307) —

I certainly don’t agree with you Larry. . . .I quoted Zachary’s first comment to show the only point that he seemed to be unsure about, (whether Cit+ was postulated at the start) and then his subsequent comment where he corrects himself (yes, but its so rare that it really wasn’t expected).

As I said, rarity or unexpectedness has nothing to do with whether or not it was a “goal.” In searches for the Lost Dutchman Mine or the ivory-billed woodpecker, finding them are “goals.”

Now can we please move on?

You can move on — I am not going to. I am not going to give up so easily after all of the time I have spent pursuing this issue. I showed that according to a standard dictionary’s definition of “goal,” Zachary made confusing, ambiguous, and inconsistent statements about whether Cit+ evolution was a “goal” of the experiment. He failed to clarify those statements. The problem is not just with this comment thread — in other discussions, he could mislead people by just saying that Cit+ evolution was never a goal. He also failed to answer my question of whether a purpose of the glucose cycling was to favor Cit+ evolution.

Larry’s finest friend
June 24, 2008

Wow! How can Fafartwat pack so much stupid into such a small brain? Especially when there’s so few functioning synapses left after his ego has swallowed so many up.

He won’t read, he can’t think, he doesn’t understand. He blames his huge inadequacies on everybody else. Does he have any positive qualities? Couldn’t evolution come up with something closer to intelligent life? Couldn’t God have created something that was less a waste of space?

Now, can we have som LOLlarries?

Lee
June 24, 2008

There are very good reasons why Fafarman has been banned from so many blogs.

Zachary has stated clearly that citrate was included as a chelating agent to assist in iron utilization. He has stated clearly that glucose cycling was included to create selection pressure for any possible mutations favoring reproduction in a carbon-limited environment. He has stated clearly that there was discussion of whether the coli would evolve an ability to utilize that energy-rich citrate – its an obvious thing to wonder about – but that it was not a goal.

Larry keeps whining that Zachary wont take hieriment was. Larry, the world does not revolve around you. Papers are pubished because a LOT of people are interested, and there isnt time in the universe to take every vain, self-glorified, uninformed idiot on the internet and carefully explain to them what they refuse to learn for themselves. There is an expectation that interested people will take the time to educate themselves, so as not to waste the time of the person who did the hard work of carrying out the experiment and COMMUNICATING IT TO THE WORLD BY PUBLISHING IT!!!!

Whining that Zachary wont communicate with you, while you continue to refuse to take advantage of the most fundamental ways in which he has communicated his work to EVERYONE, is simply self-absorbed, intellectually-lazy, time-wasting, conversation-deadening, narcissistic special pleading of the very worst sort. Shut the f*** up.

Larry Fafarman
June 24, 2008

Shut the f*** up.

Shut the f*** up yourself, you lousy sack of %$*&^@. Nothing that the paper says can change the fact that Zachary is posting bullshit on this blog and won’t answer some simple, basic questions.

He could clarify his statements by saying that Cit+ evolution was one of several goals or was a longshot goal or a secondary goal or was never considered or whatever. What if there is another discussion and he only says that Cit+ evolution was never a goal — the statement could mislead people. And he never answered my question of whether favoring Cit+ evolution was a purpose of the glucose cycling. Andy Schlafly at Conservapedia is wasting his time in his futile effort to discredit the paper by asking for all of the raw data — I have discredited the paper right here by showing that one of the principal investigators is an evasive jerk.

Carl Zimmer
June 24, 2008

Ding! Not one, but two commenters have just earned a banning. Lee for spewing obscenities, and Larry for, most recently, calling the subject of the post an evasive jerk. Au revoir.

Jacob Basson
June 24, 2008

Larry Fafarman said “I have discredited the paper right here by showing that one of the principal investigators is an evasive jerk. ”

Even if you had done such a thing (you didn’t, but you’re close: you’ve proven that YOU are a jerk), it wouldn’t discredit the paper.

Hoovooloo
June 24, 2008

Let me point out one important point of your post:

“He could clarify his statements by saying that Cit+ evolution was one of several goals or was a longshot goal or a secondary goal or was never considered or whatever.”

Did you miss it?

“or was never considered”

He did say it was never considered, when he said that Cit+ was not a goal. So, he did clarify his statement, and your comment is both stupid and meaningless. He is not being evasive, you are being willfully ignorant.

Steve
June 25, 2008

It seems to me that it makes no difference if the citrate eating behaviour was planned from the outset or not.

The key concept is that the bacteria changed from not being able to eat citrate to being able to eat citrate. No one, not even Larry, doubts this.

If this can happen in the lab with or without a bit of prodding from the experimenters then it can certainly happen outside of the lab.

Whether your world view can grow to encompass this new FACT is an entirely different story. Shooting the messenger doesn’t help.

Trevor Murray
June 25, 2008

I’m glad this thread is over and can’t wait for Zachary’s “Big post”.

Robert Carnegie
June 26, 2008

Well, I quit reading comments around eighty-something, back there, but a couple of points caught my eye:

– I hope I have read this right, apparently with inside information, our host seems to describe the experiment as just an exercise in breeding bugs that are better at eating glucose, and they are. That some of them now eat citrate came as a surprise. Better hope they don’t learn to eat glass, or they’ll break out and escape from the lab, leading to catastrophe for spectacle wearers everywhere and the collapse of civilisation (Notice how many leading world politicians wear spectacles…)

– It does seem hard to say that no other bug got in from outside the experiment and transferred some useful gene for swallowing citrate to the lab bug population – but apparently it is a combination that has never been found in the great laboratory, the natural world. Having said that, it may be a combination that is not advantageous in the natural world, only in this strange domain of glucose and citrate.

– Another point about the natural world is that E. coli apparently has been evolving there for way longer than in -this- laboratory. (Although in this laboratory it has surely mutated every single gene it has.) So a mutation that improved glucose digestion -without- impairing uptake of other materials surely would have appeared -already- in the natural world, and would have beat out the rest. So that hypothetical mutation is already present in the initial sample after all. (Unless it’s a very unlikely mutation even on the historic scale – and then it won’t happen in your lab, either.) It only remains for the laboratory bugs to find ways to use glucose better while sacrificing other processes that are important to their cousins outdoors. For instance, if the metaphor applies of the microbe having slots in its skin to take in particular shaped molecules, like a child’s block toy, then one improvement is to have more glucose-shaped slots instead of some of the other shape slots – sacrificing (partially?) the ability to use those other molecules.

W. Kevin Vicklund
June 26, 2008

- I hope I have read this right, apparently with inside information, our host seems to describe the experiment as just an exercise in breeding bugs that are better at eating glucose, and they are.

That is a gross oversimplification of the experiment, and completely misses the point. The point of the experiment was to demonstrate whether evolution is constrained to a single path. By tracking the evolution of 12 genetically identical clones* in separate but identical environments, they were able to test that question. The ability to metabolize citrate represents a spectacular confirmation that evolution can take multiple paths, but it is not the only result that confirms this.

*except for a marker demonstrated to be neutral in the experimental environment

– It does seem hard to say that no other bug got in from outside the experiment and transferred some useful gene for swallowing citrate to the lab bug population – but apparently it is a combination that has never been found in the great laboratory, the natural world. Having said that, it may be a combination that is not advantageous in the natural world, only in this strange domain of glucose and citrate.

They tested in a great many ways to make sure that nothing got in to contaminate it. While it is not an absolute certainty (no conclusion in science is), they can make that claim with greater confidence than a DNA “fingerprinting” lab could claim that your mother is in fact your mother.

Continuing the Discussion

[…] the fact of evolution. Carl Zimmer at his blog The Loom covered it quite well a few weeks back: A New Step In Evolution | The Loom | Discover Magazine Also, I think this Stephen Jay Gould quote fits the theme of this thread very well: Stephen Jay […]

[…] to pay a visit to the lab of Richard Lenski, whose work documenting evolution in action I’ve written about on the Loom and in my book Microcosm. You can read about their work in what the BBC is calling a […]

[…] were fabulous. One person got up and said she had a two-part question. She wanted me to talk about the long-term evolution experiments Richard Lenski runs with E. coli, and she wanted Susskind to talk about whether the anthropic […]

[…] It’s going to be heavily laden with cool examples from recent years, from E. coli that break all the rules to kinky ducks. If all goes according to plan, it should be out in time this fall for the 150th […]

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